Artificial intelligence (AI) is being increasingly studied and implemented in gastroenterology. In inflammatory bowel disease (IBD), numerous AI models are being developed to assist with IBD diagnosis, standardization of endoscopic and radiologic disease activity, and predicting outcomes. Further prospective, multicenter studies representing diverse populations and novel applications are needed prior to routine implementation in clinical practice and expected improved outcomes for clinicians and patients.

Primary Care is the first point of contact for most patients after the onset of symptoms of inflammatory bowel disease (IBD). Establishing an initial diagnostic process based on compatible symptoms and agreed criteria and referral pathways, depending on the degree of suspicion and the patient's situation, can reduce diagnostic delays. Once the patient is referred to the Digestive specialist and the diagnosis of IBD is established, a treatment and follow-up plan is structured. The management of the patient must be shared with the participation of the family practitioners in the diagnosis and treatment of concomitant or intercurrent pathologies, the recognition of flare-ups or complications (of IBD or treatments), education tasks or adherence control. With the purpose of developing a comprehensive guide on the management of IBD aimed at Primary Care doctors, we have developed this positioning document collaboratively between the Spanish Society of Primary Care Physicians (SEMERGEN) and the Spanish Working Group on Crohn's Disease and Ulcerative Colitis (GETECCU).

Patients with inflammatory bowel disease (IBD) have lower health-related quality of life (HRQoL) than the general population. The highest incidence and prevalence rates of IBD in the world are found in the Faroe Islands, however, the HRQoL of Faroese patients is unknown. This study aimed to determine their HRQoL at diagnosis and two years of follow-up in comparison with Danish patients.

All patients (15 years or older) were invited to answer the Short Form 12 questionnaire (SF-12) and Short Inflammatory Bowel Disease Questionnaire (SIBDQ) at diagnosis and follow-up. Faroese patients were included from 2010 to 2022, and Danish patients in 2010.

160 Faroese patients and 160 Danish patients completed questionnaires twice. For Faroese patients with IBD, the physical and mental component summary scores (SF-12) significantly improved from 46.6 and 44.0 to 49.4 and 47.7, respectively. Total SIBDQ scores also improved from 46.6 to 53.9. However, Faroese patients had significantly lower scores at diagnosis of social functioning, mental health, and mental component summary (SF-12) as well as lower emotional scores (SIBDQ) compared with Danish patients.

Faroese patients with IBD improved their HRQoL from diagnosis to follow-up, although greater improvements were observed for Danish patients. Increased awareness of the HRQoL of this patient group is warranted as Faroese patients had lower mental and emotional scores than Danish patients at diagnosis.

The aim of the present study was to assess prevalence and disease outcomes of arthritis in a nationwide cohort of pediatric patients with inflammatory bowel disease (IBD).

We collected data of pediatric IBD patients experiencing arthritis from the Italian Society of Pediatric Gastroenterology, Hepatology and Nutrition IBD registry. We gathered baseline and one-year follow-up data on concomitant IBD and arthritis diagnosis.

150 patients [(99 Crohn's Disease (CD), 51 Ulcerative Colitis (UC) and Unclassified IBD (IBDU)] with arthritis out of 3061 (1301 CD and 1760 UC) patients were identified, with an overall prevalence of 4.9 %. Arthritis was more frequent in CD than in UC (7.6 % vs 2.9 %, p < 0.01). Peripheral arthritis was more frequently diagnosed in patients with active IBD than in those with quiescent disease (94.6 % vs 67.3 %, p < 0.01). At one-year follow-up, clinically active IBD was independently associated with lower peripheral arthritis remission rates, whereas it did not impact axial arthritis remission. The presence of additional EIMs was associated with lower IBD clinical remission rates.

Clinically active IBD impacts peripheral arthritis but not axial one, whose activity appeared to be independent by intestinal disease. The presence of additional EIMs has a negative prognostic impact on IBD course.

Inflammatory bowel disease (IBD) is a chronic, immune-mediated inflammatory disorder of the gastrointestinal tract. In IBD, systemic inflammation and immune dysregulation may also impact extraintestinal organs, such as the thyroid gland. Despite this, little is known about the influence of concomitant hypothyroidism on the clinical course of IBD.

A retrospective analysis was conducted among adult patients with IBD and at least one thyroid stimulating hormone (TSH) measurement within a large healthcare network. Patient charts were reviewed, and baseline demographics, disease characteristics, biomarkers, healthcare utilization, medication use, and other comorbidities were extracted. Patients were stratified by those with IBD only and those with concomitant IBD and hypothyroidism. Multivariable logistic regression was used to identify factors associated with concomitant hypothyroidism. Concomitant disease as an independent predictor for lab abnormalities and increased healthcare utilization was also assessed using multivariable logistic and negative binomial regression.

We identified 287 adult patients with IBD, including 146 (50.9%) with Crohn's disease (CD) and 141 (49.1%) with ulcerative colitis (UC). Among this sample, 178 (62.0%) patients had concomitant hypothyroidism. Concomitant disease was associated with older age (adjOR 1.04, 95% CI 1.02, 1.06), female sex (adjOR 1.78, 95% CI 1.01, 3.16), and the presence of other extraintestinal manifestations (adjOR 2.30, 95% CI 1.06, 5.00). Concomitant disease was also found to be a significant predictor for increased healthcare utilization, specifically, higher number of radiation-based abdominal imaging (RBAI) studies (adjIRR: 1.89, 95% CI 1.08, 3.32).

Patients with both IBD and hypothyroidism have an increased likelihood of other extraintestinal manifestations compared to individuals who have IBD without hypothyroidism. Furthermore, patients with concomitant disease exhibited greater healthcare utilization, specifically, increased rates of RBAI studies. The presence of concomitant hypothyroidism may be associated with a more severe course of IBD.

Patients with inflammatory bowel disease may present with extraintestinal manifestations. Crohn's disease complicated with IgA nephropathy or IgA vasculitis is relatively rare. In this case, an 11-year-old girl was diagnosed with Crohn's disease and infliximab was administered. 1 year after treatment, she presented with asymptomatic but persistent microscopic hematuria. The child was diagnosed with IgA vasculitis and IgA nephropathy at the fourth year of follow-up. To explore the association between Crohn's disease and IgA associated diseases, immunostaining for IgA and GdIgA1 deposition was retrospectively conducted in intestinal biopsy tissues obtained at the time of initiation and relapse of Crohn's disease. GdIgA1 deposition in intestinal tissues was found not only at the time of relapse of Crohn's disease, but also at the beginning of Crohn's disease when patient had neither exposure to any drug nor any symptom of IgA vasculitis or IgA nephropathy. The early appearance of GdIgA1 deposition indicated that Crohn's disease played a greater role in its formation than infliximab induction and the child might be prone to IgA associated diseases. Patients with Crohn's disease, especially those who receive tumor necrosis factor-alpha inhibitors are recommended to receive regular kidney examinations.

Inflammatory bowel disease (IBD) is an idiopathic intestinal inflammatory condition with chronic and relapsing manifestations and is characterized by a disturbance in the interplay between the intestinal microbiota, the gut, and the brain. The microbiota-gut-brain axis involves interactions among the nervous system, the neuroendocrine system, the gut microbiota, and the host immune system. Increasing published data indicate that psychological stress exacerbates the severity of IBD due to its negative effects on the microbiota-gut-brain axis, including alterations in the stress response of the hypothalamic-pituitary-adrenal (HPA) axis, the balance between the sympathetic nervous system and vagus nerves, the homeostasis of the intestinal flora and metabolites, and normal intestinal immunity and permeability. Although the current evidence is insufficient, psychotropic agents, psychotherapies, and interventions targeting the microbiota-gut-brain axis show the potential to improve symptoms and quality of life in IBD patients. Therefore, further studies that translate recent findings into therapeutic approaches that improve both physical and psychological well-being are needed.

Visceral hypersensitivity is one of the most prevalent symptoms of inflammatory bowel disease (IBD), and it can be difficult to cure despite achieving endoscopic remission. Accumulating studies have described that macrophage colony-stimulating factor (M-CSF) modulates neuroinflammation in the central nervous system (CNS) and the development of chronic pain, while the underlying mechanism for whether and how M-CSF/CSF1R signaling pathway regulates visceral hypersensitivity following colitis remains unknown. In the present study, using the dextran sulfate sodium (DSS)-induced colitis model, we determined that microglial accumulation occurred in the spinal dorsal horn during remission phase. The reactive microglia released inflammatory factor, increased neuronal excitability in the dorsal horn, and produced chronic visceral pain behaviors in DSS-treated adult male mice. In addition, we also found significantly increased signaling mediated by astrocytic M-CSF and microglial CSF1R in dorsal horn in the mice with colitis. Exogenous M-CSF induced microglial activation, neuronal hyperactivity and behavioral hypersensitivity in the control group, inhibition of astrocyte/microglia by fluorocitrate/minocycline significantly suppressed microglial and neuronal activity, and relieved the visceral hypersensitivity in the model mice. Overall, our experimental study uncovers the critical involvement of spinal astrocyte-derived M-CSF and reactive microglia in the initiation and maintenance of visceral hypersensitivity following colitis, thereby identifying spinal M-CSF as a target for treating chronic visceral pain. This may provide more accurate theoretical guidance for clinical patients with IBD.

To investigate the causal relationship between inflammatory bowel disease (IBD) and uveitis, we conducted a two-sample bidirectional Mendelian randomization (MR) analysis utilizing summary data from genome-wide association studies (GWAS). The primary statistical analysis was performed using the inverse-variance weighted (IVW) method. False discovery rate (FDR) correction was used to control for false positives in multiple testing. In addition, sensitivity analyses were carried out using the MR Egger intercept test and Cochran's Q test. The MR analysis revealed that genetically determined IBD (OR = 1.141, 95% CI 1.080-1.205, P = 2.21 × 10-6, PFDR = 6.90 × 10-6), ulcerative colitis (UC) (OR = 1.113, 95% CI 1.032-1.201, P = 0.006, PFDR = 0.009), and Crohn's diseases (CD) (OR = 1.073, 95% CI 1.017-1.133, P = 0.010, PFDR = 0.011) had a causal effect on uveitis. Conversely, the reverse MR analysis did not reveal significant causal link of uveitis on IBD, including its two subtypes. Furthermore, the results of the MR-Egger and weighted median methods were consistent with the IVW method. No evidence of heterogeneity or pleiotropy was detected by sensitivity analysis. Our findings confirm that IBD and its main subtypes had a causal connection with uveitis. Further research is needed to elucidate the underlying pathophysiological mechanisms driving this association.

The causal relationship between inflammatory bowel disease (IBD) and diabetes mellitus remains unclear. The aim of this study was to delve into this association and investigate the correlation between AMP-activated protein kinase (AMPK), a target gene of metformin, and the risk of developing IBD. Researchers conducted a bidirectional two-sample Mendelian randomization analysis to examine causal relationships between IBD, including ulcerative colitis and Crohn disease (CD), and diabetes mellitus, encompassing both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). Additionally, this study utilized AMPK-related variants associated with HbA1c (%) as instrumental variables for the metformin target gene AMPK to further investigate their association with the risk of IBD. The inverse variance weighted method was used as the primary analytical approach. Mendelian randomization analysis revealed a suggestive association between IBD and T1DM (P = .024). CD was associated with an increased risk of T1DM (P = .011). In the reverse analysis, T1DM also increased the risk of IBD (P = .043). No causal relationship was found between IBD and T2DM in either the forward or reverse analyses. In addition, this study did not find any significant effect of AMPK on IBD. In conclusion, this study suggests a bidirectional association between IBD and T1DM, in which CD may increase the risk of T1DM. However, no causal relationship was found between IBD and T2DM. Furthermore, our findings revealed that the metformin's target gene AMPK had no significant effect on the onset of IBD.

In this article, we comment on the article by Blüthner et al. The article provides a comprehensive analysis of the factors contributing to the late detection of Crohn's disease and ulcerative colitis within a German cohort. It highlights the consequences on patient outcomes, particularly disease progression and the increased risk of developing complications. The study identifies specific predictors associated with both patient-related and physician-related delays, offering a detailed exploration of the initial approach. Additionally, the article delves into the distinct patterns observed in the German population, stressing the unique aspects of diagnostic delays that may differ from those reported in other regions. This detailed examination offers valuable insights into the specific challenges faced within the German healthcare system and underscores the necessity of targeted interventions to facilitate early diagnosis. The importance of improved screening tools, patient education, and better healthcare infrastructure is emphasized as crucial steps toward improving patient care in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a complex condition linked to the gut microbiota, host metabolism, and the immune system. Edible mushroom polysaccharides (EMPs) are gaining attention for their benefits, particularly as prebiotics that help balance gut microbial, a key factor in IBD. With their scalable production, diverse hydrophilic properties, and demonstrated anti-inflammatory effects in both laboratory and animal studies, EMPs show promise for easing IBD symptoms. By supporting a healthy gut microbiome through various mechanisms, EMPs can play an important role in preventing and managing IBD, ultimately benefiting overall health and opening new treatment avenues. This review examines how EMPs affect IBD, focusing on their role in shaping gut microbiota, restoring gut barriers, regulating immune function, and influencing pathways related to colitis. It also explores their impact on the microbiota-gut-multi organ axis and overall host health, as well as the relationship between EMPs preparation, structure, and bioactivity, along with their potential applications in food and medicine. This investigation provides valuable insights into the intricate connections between the gut, immune system, and systemic inflammation system, highlighting how EMPs are key players in this complex interaction.

Panniculitis is associated with a variety of disease processes that can be challenging to distinguish clinically. While diagnosis often relies on histopathology, sometimes this is not sufficiently diagnostic, which requires careful consideration of clinical features. We sought to provide an overview of the most common adult noninfectious panniculitis by reviewing not only the histological distinguishing features but also the clinical characteristics of various types of panniculitis including patient history, distribution, morphology, and other clues. A narrative review of both common and rare panniculitis primarily affecting the adult patient population was performed, with focus on recent English language publications. Additionally, both traditional and emerging therapeutic options are discussed. This article focused on diseases affecting predominantly adult populations and does not detail pediatric panniculitis or infectious etiologies. Overall, histopathology remains a key component in the diagnosis of panniculitis, but clinical characteristics provide substantial aid.

There is an unmet need to adequately identify, describe and treat the musculoskeletal manifestations of patients with inflammatory bowel disease (IBD). At the 2024 SPARTAN annual meeting, we reviewed the current literature on the prevalence and presentation of spondyloarthritis in patients with IBD and discussed screening strategies to select symptomatic patients for further study. The primary goal is to improve understanding and recognition of spondyloarthritis in this patient population.

In a unique collaboration between U.S. gastroenterologists and rheumatologists, the Gastroenterology and Rheumatology assessment of Spondyloarthritis in Inflammatory Bowel Disease (GRaSp-IBD) study group designed and executed a multi-center study across six institutions that applied a hybrid screening tool to identify patients with musculoskeletal symptoms suggestive of spondyloarthritis. The data was analyzed for confirmed rheumatic disease, treatment history, patient and IBD characteristics. Of the patients that screened positive, the majority (69%) had not seen a rheumatologist within the past year. IBD phenotype did not seem to increase the risk of a positive screen, but a higher number of biologic exposures proved significant. IBD patients report musculoskeletal pain at a high rate but a minority of these patients are seen by rheumatologists. Further study is needed to determine how to optimize screening for IBD arthritis, and to improve referral rates and clinical outcomes.

Inflammatory bowel disease (IBD) related arthritis is the most prevalent extraintestinal manifestation (EIM) of IBD, ranging between 10 and 39%. Magnetic resonance enterography (MRE) is used to assess small bowel disease involvement in Crohn's disease (CD) and can detect signs of sacroiliitis in up to 23.5% of patients. The predicting role of sacroiliitis detected on MRE is still unknown. The aim of this study is to evaluate the predictive role of sacroiliitis at MRE and other clinical features for IBD-related arthritis development in a cohort of adult patients with CD.

Between December 2012 and May 2020, consecutive patients with CD who performed MRE were enrolled in the study. Patients with a previous diagnosis of IBD-related arthritis were excluded. A baseline demographics and clinical characteristics of the patients were retrospectively collected. The identification of new-onset IBD-related arthritis events during the follow-up was based on rheumatological clinical diagnosis and fulfillment of the ASAS classification criteria.

Ninety-five patients, mean age 43.9 years (standard deviation [SD] ± 16.6), 52.6% female were enrolled in the study with a median follow-up of 83 months (Q25:75 25:143). Six out 95 (6.3%) developed IBD-related arthritis with a mean time of 11 months (SD ± 16.8). Sacroiliitis detected on MRE was not associated with an increased risk of IBD-related arthritis (odds ratio [OR] = 2.12 [95% confidence interval (CI) 0.36, 12.53, p = 0.408]). In contrast, the presence of arthralgia and EIMs were found to be a predictor for IBD-related arthritis development (OR = 84.0 [95% CI 8.18, 862.39, p < 0.0001] and OR = 7.37 [95% CI 1.25, 43.32, p = 0.027], respectively).

This study highlights that sacroiliitis, as assessed by MRE, was not associated with the development of IBD-related arthritis, whereas extraintestinal manifestations and arthralgia were significantly associated with later IBD-related arthritis development in patients with CD.

The enzyme N-acetyltransferase 2 (NAT2) plays an important role in metabolism and detoxification of xenobiotics, including carcinogens and medications. We aimed to assess the contribution of the NAT2 polymorphism to susceptibility to inflammatory bowel disease (IBD) in the Polish population. The study involved 101 IBD patients and 100 healthy controls. The NAT2 gene mutations at positions 481T, 803G, 590A, and 857A were identified using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique on peripheral blood DNA samples. Carriers of the NAT2*5 allele had a greater chance of developing Crohn's disease (CD) (OR = 1.73, 95% CI 1.06-2.83). Also, the NAT2*4/5 genotype was more prevalent in CD patients (OR = 2.77, 95% CI 1.17-6.57). When compared to the control group, the prevalence of the NAT2*4/6 genotype in the IBD patient population was significantly lower (10.9% vs. 30.0%, p < 0.01). In the Polish population, polymorphism in the NAT2 gene may potentially alter susceptibility to IBD.

The structural disruption of intestinal barrier and excessive reactive oxygen/nitrogen species (RONS) generation are two intertwined factors that drive the occurrence and development of ulcerative colitis (UC). Synchronously restoring the intestinal barrier and mitigating excess RONS is a promising strategy for UC management, but its treatment outcomes are still hindered by low drug accumulation and retention in colonic lesions. Inspired by intestine colonizing bacterium, we developed a mucoadhesive probiotic Akkermansia muciniphila-mimic entinostat-loaded hollow mesopores prussian blue (HMPB) nanotherapeutic (AM@HMPB@E) for UC-targeted therapy via repairing intestinal barrier and scavenging RONS. After oral administration, the negatively charged AM@HMPB@E specifically bind to the positively charged inflamed colon lesions via electrostatic interactions and Akkermansia muciniphila membrane-mediated bioadhesion mechanism. Subsequently, the superoxide dismutase (SOD)-, and catalase (CAT)-like HMPB eliminated RONS, thereby alleviating RONS-mediated inflammation and intestinal epithelial damage. Meanwhile, the UC-site locally released entinostat could repair the damaged intestinal epithelial barrier by inhibiting intestinal endothelial cell apoptosis and up-regulating the expression of tight junctions. Both in vitro and in vivo results shown that AM@HMPB@E not only exhibited an exceptional retention in the colitis site but also demonstrated superior therapeutic efficacy compared to the first-line drug sulfasalazine, as evidenced by the longer colon, less rectal bleeding and body weight loss. Collectively, our findings highlight the clinical application prospects of this synchronous nanotherapeutic strategy for UC treatment, offering a paradigm for the rational design of oral nanomedicine.

Background/Objectives: Current inflammatory bowel disease (IBD) treatments focus on symptomatic relief, highlighting the need for innovative approaches. Dysregulation of the cannabinoid 1 (CB1) receptor, part of the endocannabinoid system, is linked to colitis. While tetrahydrocannabinol (THC) alleviates colitis via CB1 activation, its psychotropic effects limit clinical use. ZCZ011, a CB1R allosteric modulator, and cannabidiol (CBD), a non-psychoactive cannabinoid, offer alternatives. This study investigated combining sub-therapeutic THC doses with ZCZ011 or CBD in a murine model of dextran sodium sulphate (DSS)-induced colitis. Methods: Acute colitis was induced with 4% DSS for 7 days, followed by 3 days of water. Chronic colitis was modelled over 24 days with alternating DSS concentrations. The combination of 2.5 mg/kg THC with 20 mg/kg ZCZ011 or 10 mg/kg CBD was evaluated. Key markers were assessed to determine efficacy and safety, including disease activity index (DAI), inflammation, cytokine levels, GLP-1, and organ health. Results: DSS-induced colitis resulted in increased DAI scores, cytokines, organ inflammation and dysregulation of GLP-1 and ammonia. THC at 10 mg/kg significantly improved colitis markers but was ineffective at 2.5 and 5 mg/kg. ZCZ011 alone showed transient effects. However, combining 2.5 mg/kg THC with either 20 mg/kg ZCZ011 or 10 mg/kg CBD significantly alleviated colitis markers, restored colon integrity and reestablished GLP-1 homeostasis. This combination also maintained favourable haematological and biochemical profiles, including a notable reduction in colitis-induced elevated ammonia levels. Conclusions: This study demonstrates the synergistic potential of low-dose THC combined with CBD or ZCZ011 as a novel, effective and safer therapeutic strategy for ulcerative colitis.

Primary Care is the first point of contact for most patients after the onset of symptoms of inflammatory bowel disease (IBD). Establishing an initial diagnostic process based on compatible symptoms and agreed criteria and referral pathways, depending on the degree of suspicion and the patient's situation, can reduce diagnostic delays. Once the patient is referred to the Digestive specialist and the diagnosis of IBD is established, a treatment and follow-up plan is structured. The management of the patient must be shared with the participation of the family practitioners in the diagnosis and treatment of concomitant or intercurrent pathologies, the recognition of flare-ups or complications (of IBD or treatments), education tasks or adherence control. With the purpose of developing a comprehensive guide on the management of IBD aimed at Primary Care doctors, we have developed this positioning document collaboratively between the Spanish Society of Primary Care Physicians (SEMERGEN) and the Spanish Working Group on Crohn's Disease and Ulcerative Colitis (GETECCU).

Previous studies have suggested an association between inflammatory bowel disease (IBD), and pancreatitis, including acute pancreatitis (AP) and chronic pancreatitis (CP). We aimed to examine the potential causal relationship between IBD and pancreatitis using the Mendelian randomization (MR) method.

We obtained data from genome-wide association studies (GWASs) in European individuals for IBD and its main subtypes, Crohn's disease (CD) and ulcerative colitis (UC) (31,665 IBD cases, 13,768 UC cases, 17,897 CD cases and 33,977 controls). Four independent summary statistics of pancreatitis from the the European Bioinformatics Institute (EMBL-EBI, 10,630 AP cases and 844,679 controls, 1,424 CP cases and 476,104 controls) and FinnGen Consortium (8,446 AP cases, 4,820 CP cases and 437,418 controls) were used for bidirectional MR analyses and sensitivity analysis. Finally, further meta-analysis was conducted on the MR results.

Generally, IBD is associated with an increased risk of pancreatitis (IBD-AP, OR = 1.050, 95% CI 1.020-1.080, P = 7.20 × 10-5; IBD-CP, OR = 1.050, 95% CI 1.010-1.090, P = 0.019). In addition, UC increased the risk of pancreatitis (UC-AP, OR = 1.050, 95% CI 1.020-1.070, P = 9.10 × 10-5; UC-CP, OR = 1.090, 95% CI 1.040-1.140, P = 1.44 × 10-4) and CD increased the risk of acute pancreatitis (OR = 1.040, 95% CI 1.020-1.060, P = 9.61 × 10-5). However, no causal association was found between CD and the risk of chronic pancreatitis (P > 0.05). The reverse MR results showed that AP may be associated with a reduced risk of IBD and CD (AP-IBD, OR = 0.880, 95% CI 0.810-0.960, P = 0.003; AP-CD, OR = 0.830, 95% CI 0.730-0.940, P = 0.003). However, there is no causal relationship between AP and the risk of UC, and there is no causal relationship between CP and the risk of IBD and its subtypes(P > 0.05).

In conclusion, based on MR analysis and meta-analysis, our results showed a positive causal effect of IBD on pancreatitis, and subgroup analyses showed that UC and CD may promote the development of acute pancreatitis, whereas UC may promote the development of chronic pancreatitis. Reverse MR analysis suggests that AP may have a potential protective effect on IBD and CD.

Background/Objectives: Inflammatory bowel disease (IBD) is a persistent inflammatory condition affecting the gastrointestinal tract, distinguished by the impairment of the intestinal epithelial barrier, dysregulation of the gut microbiota, and abnormal immune responses. Cajanus cajan (L.) Millsp., traditionally used in Chinese herbal medicine for gastrointestinal issues such as bleeding and dysentery, has garnered attention for its potential therapeutic benefits. However, its effects on IBD remain largely unexplored. Methods: In this study, the major compounds from Cajanus cajan leaf extract (CCLE) were initially characterized by LCMS-IT-TOF. The IBD model was developed in C57BL/6 mice by administering continuous 4% (w/v) dextran sodium sulfate (DSS) aqueous solution over a period of seven days. The body weight, colon length, disease activity index (DAI), and histopathological examination using hematoxylin and eosin (H&E) staining were performed in the IBD model. The levels of the main inflammatory factors, specifically TNF-α, IL-1β, IL-6, and myeloperoxidase (MPO), were quantified by employing enzyme-linked immunosorbent assay (ELISA) kits. Additionally, the levels of tight junction proteins (ZO-1, Occludin) and oxidative stress enzymes (iNOS, SOD1, CAT) were investigated by qPCR. Subsequently, flow cytometry was employed to analyze the populations of various immune cells within the spleen, thereby assessing the impact of the CCLE on the systemic immune homeostasis of IBD mice. Finally, 16S rDNA sequencing was conducted to examine the composition and relative abundance of gut microbiota across different experimental groups. In addition, molecular docking analysis was performed to assess the interaction between the principal components of CCLE and the aryl hydrocarbon receptor (AHR). Results: We identified seven bioactive compounds in CCLE: catechin, cajachalcone, 2-hydroxy-4-methoxy-6-(2-phenylcinyl)-benzoic acid, longistylin A, longistylin C, pinostrobin, amorfrutin A, and cajaninstilbene acid. Our results demonstrated that oral administration of CCLE significantly alleviates gastrointestinal symptoms in DSS-induced IBD mice by modulating the balance of gut-derived pro- and anti-inflammatory cytokines. This modulation is associated with a functional correction in M1/M2 macrophage polarization and the Th17/Treg cell balance in splenic immune cells, as well as shifts in the populations of harmful bacteria (Erysipelatoclostridium and Staphylococcus) and beneficial bacteria (Odoribacter, unidentified Oscillospiraceae, Lachnoclostridium, and Oscillibacter) in the gut. Furthermore, cajaninstilbene acid, longistylin A, and longistylin C were identified as potential AhR agonists. Conclusions: The present results suggested that CCLE, comprising stilbenes like cajaninstilbene acid, longistylin A, and longistylin C, protects the epithelial barrier's structure and function against DSS-induced acute IBD by restoring gut microbiota balance and systemic immune response as AhR agonists. Overall, CCLE represents a promising natural product-based therapeutic strategy for treating IBD by restoring gut microbiota balance and modulating systemic immune responses.

Inflammatory bowel disease (IBD) is a multisystem condition that could affect the cutaneous systems, namely cutaneous extraintestinal manifestations (EIMs). It has been suggested that IBD is associated with erythema nodosum (EN), malignant melanoma (MM) and non-melanoma skin cancer (NMSC). However, the potential causal relationship between IBD and the mentioned above cutaneous EIMs is still unclear. This study aims to determine the effect of IBD on EN, MM and NMSC within a Mendelian randomization (MR) design. Summary-level data for IBD, EN, MM, NMSC were obtained from large-scale genome-wide association studies. We utilized five different methods, including the inverse variance weighted model (IVW), MR Egger, Weighted median, Simple mode, Weighted mode in the MR analysis, then the Cochran's Q test, the MR-Egger pleiotropy test, the MR-PRESSO global pleiotropy test and leave-one-out sensitivity test were used to evaluate the heterogeneity and pleiotropy of identified IVs. To further ensure the validity of our findings, we evaluated the strength of the instrumental variables using the F-statistic and estimated the statistical power of our study. Findings were verified using an independent validation dataset, as well as through different MR methods with different model assumptions. MR analysis suggested that genetically determined IBD had a detrimental causal effect on NMSC (IVW: odds ratio [OR] = 1.002037, 95% confidence interval [CI] = 1.0001150-1.003962, P = 0.03776677), but not on EN (IVW: [OR] = 1.0937191, 95% [CI] = 0.9685831-1.235022, P = 0.1484349) and MM (IVW: [OR] = 0.9998064, 95% [CI] = 0.9994885-1.000124, P = 0.2326482). Besides, a positive causal effect of IBD on NMSC was verified in an independent validation dataset (IVW: [OR] = 1.002651, 95% [CI] = 1.0006524-1.004654, P = 0.009307506). The present study corroborated the causal relationship between IBD and NMSC. In contrast, our results showed no evidence of a causal association of IBD on EN and MM. These findings provide new insights into increasing attention to patients with IBD to prevent concurrent NMSC.

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), can affect the hepatobiliary system and pancreas, substantially impacting the life quality of patients.

To evaluate the quality of evidence and comprehensively assess the validity of associations of IBD with hepatobiliary and pancreatic diseases.

We performed an umbrella review of existing meta-analyses in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) recommendations.

We systematically searched PubMed, Embase, and Web of Science from inception to April 2024, to identify and appraise meta-analyses examining IBD and risk of hepatobiliary and pancreatic manifestations. Methodologic quality was assessed with A Measurement Tool to Assess Systematic Reviews (AMSTAR 2) and the strength of evidence was graded according to prespecified criteria.

A total of 14 meta-analyses of observational studies were included. The strongest-validity evidence suggested the significant associations between IBD and risk of gallstones (odds ratio (OR) = 1.72; 95% confidence interval (CI) = 1.40-2.12) and acute pancreatitis (OR = 3.11; 95% CI = 2.93-3.30). Highly suggestive evidence indicated a significantly increased risk of hepatobiliary cancer in UC (incidence rate ratio (IRR) = 2.05; 95% CI = 1.52-2.76) and CD (IRR = 2.31; 95% CI = 1.25-4.28). In addition, highly suggestive evidence indicated that IBD was associated with portal venous system thrombosis. Suggestive evidence showed a significantly higher prevalence of primary sclerosing cholangitis, non-alcoholic fatty liver disease, autoimmune hepatitis, and autoimmune pancreatitis in IBD patients than in the general population.

The associations between IBD and multiple hepatobiliary and pancreatic disorders showed varying levels of evidence and magnitude of risk. Further high-quality primary studies are needed to identify IBD patients who are more at risk and would benefit the most from screening and prevention programs.

CRD42023451461.

The development of diseases with a possible autoimmune pathogenesis is common in adults with inflammatory bowel disease (IBD). In early onset IBD, it may differ but the evidence is sparse. We aimed to investigate the risk and time span from IBD diagnosis to outcomes with different associated disorders with possible autoimmune pathogenesis.

A register-based study included all Danish patients with early onset of IBD (≤18 years) between 1980 and 2021 and 50 matched references without IBD for each case. We examined the risk of type 1 and type 2 diabetes, celiac disease, thyroid disease, rheumatoid arthritis, psoriatic arthritis, and spondyloarthritis in Cox regression models.

In total, 6822 patients with IBD were identified, and 337 728 matched references. The median age at the time of IBD diagnosis or index date for the matched references was 16 years (25-75 percentile: 13-18 years), and the median age at the time of an outcome or at the end of follow-up was 28.1 years (25-75 percentile: 21.5-37.0 years). According to the cumulative incidence plots psoriatic arthritis, and spondyloarthritis was diagnosed approximately 10 years after the IBD onset, and the remaining outcomes later. The adjusted hazard ratio after full follow-up was 4.72 (95% CI, 3.85-5.80) for psoriatic arthritis, 5.21 (95% CI, 4.17-6.50) for spondyloarthritis, 2.77 (95% CI, 1.92-4.00) for celiac disease, 2.15 (95% CI, 1.54-3.01) for rheumatoid arthritis, 1.69 (95% CI, 1.23-2.32) and 1.64 (95% CI, 1.21-2.21) for type 1 and type 2 diabetes, respectively. For thyroid disease, it was 1.16 (95% CI, 0.97-1.40).

The risk estimates were significantly increased for all outcomes at the end of follow-up, except for thyroid disease, but according to the cumulative incidence plots, only psoriatic arthritis and spondyloarthritis occurred earlier in the IBD cohort than in the matched references.

Ulcerative colitis (UC) is a chronic immune disease that is difficult to cure. We recently found that chick early amniotic fluid (ceAF) has notable anti-inflammatory and antioxidative properties, through its active components. This study demonstrates the potential of ceAF as a protective agent against UC. UPLC-MS mass spectrometry identified key components of ceAF, including various fatty acids and nucleosides. In vitro, ceAF improved viability in DSS-induced Caco-2 cells, reduced pro-inflammatory cytokines IL-1β and TNF-α, and increased the anti-inflammatory cytokine IL-10. It also upregulated the tight junction proteins ZO-1 and occludin. In DSS-induced UC mice, ceAF treatment alleviated weight loss, colon shortening, and disease activity, while improving histopathology, crypt depth, and colonic fibrosis. Mechanistically, ceAF's anti-inflammatory effects are mediated by inhibiting the overactivation of TCR signaling through the LCK/ZAP70/LAT pathway. Our findings suggest that ceAF could be a valuable nutritional intervention for UC, potentially enhancing existing functional foods aimed at managing this condition.

Spondyloarthritis (SpA) is the most common extraintestinal manifestation of inflammatory bowel disease (IBD). The application of screening tools to detect SpA in patients with IBD may lead to earlier recognition of SpA and affect treatment decisions.

A combination of two previously described SpA screening questionnaires, the Detection of Arthritis in Inflammatory Bowel Disease (DETAIL) and IBD Identification of Spondyloarthritis Questionnaire (IBIS-Q), was administered to consecutive patients with IBD attending IBD specialty clinics in six US academic medical centers. Demographic data, IBD, and rheumatology history were extracted by chart review.

A total of 669 patients were analyzed. The median age was 40 years (interquartile range [IQR] 30-54) with a median disease duration of 12 years (IQR 6-22) and moderate to severe IBD based on medication exposure and history of bowel surgery. A total of 81 patients (12%) carried a diagnosis of an inflammatory rheumatic disease, whereas 75 (11%) had consulted a rheumatologist during the previous year. Using published cutoffs, 180 out of 669 patients (27%) screened positive with DETAIL, 266 (40%) with IBIS-Q, and 275 (41%) with either questionnaire. Axial symptoms were more frequently reported than peripheral musculoskeletal complaints. Notably, 189 out of 275 (69%) screen-positive patients had neither a documented inflammatory rheumatic disease diagnosis nor a visit with a rheumatologist within the past year.

A substantial proportion of patients with IBD have symptoms suggestive of SpA, and many of these may have undiagnosed SpA. The IBIS-Q questionnaire appears to identify more potential SpA cases than DETAIL. Strategies are needed to prioritize rheumatology consultations for those patients with IBD who are most likely to benefit.

Artemisia ordosica Krasch, a traditional Chinese herbal medicine, possesses antibacterial, antiviral, and anti-inflammatory properties. The aim of this experiment was to investigate the therapeutic effect of Artemisia ordosica Krasch extraction (AOE) in treating colitis induced by dextran sulfate sodium (DSS) in mice. The in vitro antioxidant activity of AOE was evaluated by assessing its iron reduction capacity and scavenging capacity towards 1,1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl radicals (·OH). The protective effect of AOE on colitis in mice was determined by monitoring key indicators such as body weight, colon length, and survival rate in mice, as well as by assessing the expression of colon-related genes and cytokine levels. We evaluated the impact of AOE on intestinal microbiota by measuring the 16s sequencing of cecal contents and bile acid metabolism. The results showed that the iron reduction capacity of AOE was positively correlated with its concentration. The half-maximal inhibitory concentrations (IC50) for scavenging DPPH and hydroxyl radicals were 3.126 mg/mL and 6.139 mg/mL, with a 95% confidence interval of 95%. In vivo studies demonstrated that AOE reduced DSS-induced colitis in mice by increasing the colon length, enhancing antioxidant enzyme activity, inhibiting inflammatory cell infiltration, suppressing the formation of TNF-α and IL-6, and reducing malondialdehyde (MDA) levels. qPCR analysis revealed that AOE reversed the down-regulation of Claudin mRNA expression, and altered the composition of cecal microbiota, thus mitigating DSS-induced colitis. AOE plays a crucial role in alleviating colitis in mice and effectively improves DSS-induced colitis, highlighting its potential as a therapeutic agent for inflammatory bowel diseases.

The introduction of tumor necrosis factor inhibitors has led to a paradigm shift in the management of inflammatory bowel disease (IBD). The subsequent introduction of both anti-integrins and cytokine blockers has since expanded the biologic armamentarium. However, immunogenicity, defined as the production of anti-drug antibodies (ADAs) to the prescribed biopharmaceutical, means a significant fraction of patients exposed to biologic agents will experience a secondary loss of response to one or more of the drugs. In clinical settings, immunogenicity may be caused by several factors, both patient related (e.g., underlying chronic disease, systemic immune burden, including previous biologic therapy failure, and [epi]genetic background) and treatment related (e.g., dose and administration regimens, drug physical structure, photostability, temperature, and agitation). Here, we outline these elements in detail to enhance biopharmaceutical delivery and therapy for patients with IBD. Moreover, concurrent immunomodulator medication may reduce the risks of ADA generation, especially when using the chimeric drug infliximab. Summarizing the latest developments and knowledge in the field, this review aims to provide strategies to prevent ADA production and information on managing non-responsiveness or loss of response to biologics. Better understanding of the molecular mechanisms underlying the formation of ADAs and the critical factors influencing the immunogenicity of biopharmaceuticals may lead to improved health outcomes in the IBD community that may benefit both the individual patient and society through lower healthcare expenses.

Inflammatory bowel disease (IBD) is associated with extraintestinal manifestations that can affect multiple body systems. Extraintestinal manifestations (EIMSs) are seen in up to 50% of patients with IBD. Skin involvement is particularly common occurring in up to 15%-20% of patients. Skin reactivity presents in multiple forms with unique pathology. Therapy for IBD also may affect the skin directly through inflammatory processes or indirectly because of skin infections. This review will concentrate on the most common nonmalignant dermatologic conditions associated with IBD with a focus on prevalence, diagnostic approaches, and management strategies.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and risk of malnutrition can coexist in patients with inflammatory bowel disease (IBD). We performed a malnutrition risk assessment as part of the standard follow-up of IBD patients and studied the potential risk factors for being at risk of malnutrition based on the presence or absence of MASLD.

The Malnutrition Universal Screening Tool (MUST) was used to screen malnutrition risk (MUST ≥1) and controlled attenuation parameter (CAP ≥248 dB/min) to assess MASLD. Adherence to a Mediterranean diet, physical activity, and quality of life were also assessed.

Of 686 evaluated IBD patients, 130 (18.9%) were identified as being at risk of malnutrition. Patients without MASLD (n = 89 [68.5%]) were more likely to be at risk than those with MASLD (n = 41 [31.5%], p = 0.005). However, among patients at risk of malnutrition, those with MASLD were more likely to have active IBD (82.9%) than patients without MASLD (39.3%, p < 0.001). Female sex (OR 1.984, p = 0.027) and young age (OR 1.014, p = 0.006) were associated with malnutrition risk only in patients with IBD without MASLD. Being at risk of malnutrition was associated with worse quality of life (p < 0.001), especially in IBD patients with MASLD.

Malnutrition risk and quality of life are modified by the presence of MASLD in IBD patients.

Crohn's disease is known for being associated with an abnormal composition of the bacterial flora, dysbiosis and intestinal function disorders. Metabolites produced by gut microbiota play a pivotal role in the pathogenesis of CD, and the presence of unspecific extraintestinal manifestations.

The aim of this study was a determination of the level of bacterial metabolites in blood plasma in patients with Crohn's disease. CD patients (29) and healthy individuals (30) were recruited for this study. Bacterial metabolites (SCFAs and TMAO panel) were measured by a liquid chromatography-mass spectrometry system.

A significant correlation (p-value < 0.05) between CD and bacterial metabolites was obtained for three of eight tested SCFAs; acetic acid (reduced in CD; FC 1.7; AUC = 0.714), butyric acid (increased; FC 0.68; AUC = 0.717), 2MeBA (FC 1.168; AUC = 0.702), and indoxyl (FC 0.624). The concentration of CA (FC 0.82) and choline (FC 0.78) in plasma was significantly disturbed according to the biological treatment. Choline level (FC 1.28) was also significantly disturbed in the patients treated with glucocorticoids. In total, 68.97% of Crohn's patients presented extraintestinal manifestations (EIMs) of Crohn's disease, mainly osteoarticular complications. The level of BA was statistically significantly elevated in patients with extraintestinal (FC 0.602) manifestations, while in the group of patients with osteoarticular complications, a significant difference in the level of betaine (FC 1.647) was observed.

The analyzed bacterial metabolites of plasma may significantly help in the diagnostic process, and in the monitoring of the disease course and treatment, in a lowly invasive way, as biomarkers after additional research on a larger group of patients.

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is an autoimmune disease that is challenging to treat. This study aimed to identify the effect of sodium ferulate on endothelial dysfunction mediated by neutrophil extracellular trap (NET)-platelet activation in AAV to provide potential strategies for AAV treatment.

An animal model of myeloperoxidase (MPO)-AAV passive immune vasculitis was established using anti-MPO immunoglobulin G and Rag2 knockout mice. The efficacy and mechanism of action of sodium ferulate in AAV were explored in cultured and isolated endothelial progenitor cells (EPCs), and messenger ribonucleic acid gene expression, relative protein expression, and protein fluorescence intensity were determined through quantitative polymerase chain reaction, Western blotting, and immunofluorescence, respectively. Serum antibody concentrations were determined by enzyme-linked immunosorbent assay, and flow cytometry was used in determining the expression levels of platelet-selectin (CD62p) and procaspase-activating compound-1 (PAC-1) on the surfaces of the platelets. The EPCs' ultramicroscopic structure was observed through transmission electron microscopy.

The expression levels of ANCA, histone H3 citrullinated, and MPO protein fluorescence intensity in MPO-AAV mice were inhibited by sodium ferulate, and the expression levels of CD62p and PAC-1 on the cell surface were reduced. The relative expression levels of β-trace protein (β-TG), soluble thrombomodulin, inducible nitric oxide synthase (iNOS), and tumor necrosis factor α decreased. We found that sodium ferulate inhibited NETs' free DNA and mitigated damage in EPCs. In addition, relative expression levels of von Willebrand Factor, β-TG, and iNOS and serum concentrations of PAC-1, β-TG, and iNOS were inhibited.

Sodium ferulate can treat AAV by inhibiting NET release and platelet activation and reducing endothelial cell damage.

Plant-derived exosome-like nanoparticles (PELNs) have received widespread attention in treating ulcerative colitis (UC). However, the role of Houttuynia cordata-derived exosome-like nanoparticles (HELNs) in UC remains unclear. This study aims to evaluate the efficacy of HELNs in treating colitis in mice and investigate its potential mechanisms.

HELNs were isolated from H. cordata for characterization, and their safety and stability were evaluated. A dextran sulfate sodium (DSS)-induced colitis mouse model was utilized to assess the therapeutic potential of HELNs in UC. In vivo, imaging and flow cytometry were utilized to investigate the targeting effect of HELNs on inflamed colonic sites and their modulation of the immune environment. RNA-seq analysis and molecular docking were performed to identify potential pathways recruited by HELNs. Guided by transcriptomic findings, NLRP3-/- mice were used in conjunction with Western blotting, qPCR, immunofluorescence, and other techniques to verify that HELNs alleviated DSS-induced colitis by inhibiting NLRP3/NOD-like receptor signaling pathways. Lastly, the impact of HELNs on the gut microbiota was investigated through 16S rRNA sequencing.

HELNs significantly reduced the severity of DSS-induced colitis in mice, alleviating colitis symptoms and histopathological damage. Furthermore, HELNs can specifically target inflamed colon tissue, regulate the immune environment, and decrease inflammation. RNA-seq analysis, coupled with the use of NLRP3-/- mice, demonstrated that HELNs inhibited the NLRP3/NOD-like receptor signaling pathways. Lastly, HELNs balanced the gut microbiota composition in mice with colitis, decreasing the abundance of harmful bacteria and increasing the abundance of beneficial bacteria in the intestinal tract of these mice.

In summary, HELNs exhibit the potential to protect the colon from DSS-induced damage by inhibiting the NLRP3/NOD-like receptor signaling pathway and modulating the gut microbiota, presenting a promising therapeutic option for the management of UC.

Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease which is closely related with the overproduced reactive oxygen species (ROS), increased pro-inflammatory cytokines and disordered intestinal microbes. However, current therapeutic methods usually ignored the interrelation among the pathogenesis, and mainly focused on a single factor, inducing clinical outcomes unsatisfied. Herein, biocompatible infinite coordination polymers of drugs (Ce-SASP-RS ICPs) composed of Ce ions, FDA-approved drug sulfasalazine (SASP) and natural ingredient resistant starch (RS) were developed for synergistic treatment of IBD. The proper Ce3+/Ce4+ ratio in Ce-SASP-RS ICPs can endow them with SOD-like activities, POD-like activities and •OH scavenging ability, which guarantee Ce-SASP-RS ICPs to simultaneously kill bacteria and maintain ROS balance through cascade reactions. Owing to the recovered redox balance microenvironment, SASP in Ce-SASP-RS ICPs can better play their anti-inflammatory function. Moreover, benefitting from the recovered metabolic balance of ROS and inflammatory cytokines in colon, resistant starch can also function better in modifying gut microbiota through generating short-chain fatty acids. Collectively, Ce-SASP-RS ICPs can synergistically restore intestinal metabolic microenvironment through modulating redox balance, attenuating inflammation and modifying intestinal flora. Hence, in view of the mutual influences among IBD pathogenesis, this work presents a synergistic intervention approach for effectively treating IBD.

Inflammatory bowel disease (IBD) is a complex, multisystemic disease and is associated with ocular pathology in 4-12% of patients. In general, ocular disease affects Crohn's patients more frequently than those with ulcerative colitis. Episcleritis and uveitis are the most common presentations, with episcleritis often correlating with IBD flares, whereas uveitis presents independently of IBD activity and, in some cases, may even alert clinicians to a new diagnosis of IBD. Corneal EIMs encompass a range of pathologies, such as the common and benign keratoconjunctivitis sicca (dry eye disease), which nevertheless causes significant patient discomfort, and the rarer condition of peripheral ulcerative keratitis, which warrants urgent review due to the risk of corneal perforation. Alongside EIMs, clinicians should also be aware of the iatrogenic consequences to the eye following treatment of IBD. Corticosteroids may cause cataracts, glaucoma, and-indirectly via hyperglycaemia-diabetic retinopathy. Methotrexate is irritating to ocular tissues and may cause conjunctivitis and blepharitis. Biologic medications, such as anti-TNFα agents, overlap in their use as treatment of both IBD and uveitis, and yet in some patients may also increase the risk of acute uveitis flares, as well as opportunistic, sight-threatening infections. With integrated care between gastroenterology and ophthalmology, patient outcomes can be improved by facilitating earlier detection and management of ocular disease. This narrative review summarises the ocular extraintestinal manifestations of IBD, including pathophysiology, epidemiology, and current treatment strategies.

Background: Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, primarily affects the gastrointestinal tract. Additionally, extraintestinal manifestations may occur in the liver, musculoskeletal system and eyes. Its etiology remains unknown, and further research is required in order to develop pharmacological drugs which achieve complete remission of the pathology. Objective: The aim of this study was to analyze the incidence of ocular extraintestinal manifestations in IBD patients. Methods: A total of six searches were carried out on the medical publication server "PubMed" in June and July 2024, using different keywords; a total of 323 results were obtained, of which 34 were finally selected for study. Results: Ocular extraintestinal manifestations in IBD patients are more common in the anterior pole of the eye, with uveitis, scleritis and episcleritis being the most usual ones. In the case of the posterior pole, the most common manifestations are posterior uveitis and optic neuritis. Conclusions: The incidence of ocular complications whose origin is inflammatory, such as uveitis, scleritis, episcleritis and neuritis, is higher than that of complications of non-inflammatory origin.

Inflammatory Bowel Disease (IBD), which includes Crohn's disease and ulcerative colitis, represents a complex and growing global health issue with a multifaceted origin. This review delves into the intricate relationship between gut microbiota, autophagy, and the development of IBD. The gut microbiota, a diverse community of microorganisms, plays a vital role in maintaining gut health, while imbalances in this microbial community, known as dysbiosis, are linked to IBD. Autophagy, a process by which cells recycle their components, is essential for gut homeostasis and the regulation of immune responses. When autophagy is impaired and dysbiosis occurs, they individually contribute to IBD, with their combined impact intensifying inflammation. The interconnectedness of gut microbiota, autophagy, and the host's immune system is central to the onset of IBD. The review also examines how diet influences gut microbiota and its subsequent effects on IBD. It highlights the therapeutic potential of targeting the microbiota and modulating autophagic pathways as treatment strategies for IBD. Understanding these interactions could lead to personalized therapies within the rapidly advancing fields of microbiome research and immunology.