• Biomarkers
• Immune microenvironment
• Mendelian randomization
• Nicotinamide adenine dinucleotide
• Single-cell RNA-seq
• Ulcerative colitis

• Humans
• Colitis, Ulcerative/genetics
• Colitis, Ulcerative/diagnosis
• NAD/metabolism
• Transcriptome
• Biomarkers/metabolism
• Mendelian Randomization Analysis
• Single-Cell Analysis
• RNA-Seq
• Gene Expression Profiling
• Machine Learning
• Computational Biology/methods
• Single-Cell Gene Expression Analysis
• NADPH Oxidases

• IBD
• Machine Learning
• PWAS

• P30 DK052574 NIDDK NIH HHS
• T32 DK077653 NIDDK NIH HHS

• Adult
• Humans
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/genetics
• Colitis, Ulcerative/drug therapy
• Crohn Disease/diagnosis
• Crohn Disease/genetics
• Crohn Disease/drug therapy
• Retrospective Studies
• RNA, Small Untranslated
• Inflammatory Bowel Diseases/drug therapy
• MicroRNAs/genetics
• Biomarkers

• Aage Louis Hansen fonden
• Herlev internal research
• Colitis-Crohn Foreningen
• Torben og Alice Frimodts Fond
• Aase and Ejnar Danielsen's Foundation

• Bioinformatics
• Biomarkers
• Deep learning model
• Immune infiltration
• Machine learning
• Ulcerative colitis

• Humans
• Colitis, Ulcerative/genetics
• Dual Oxidases
• Matrix Metalloproteinase 10
• Machine Learning
• Biomarkers
• Computational Biology

• transcriptomics
• gene expression analysis
• genetics
• molecular biology
• biomarkers
• diseases
• gastroenterology
• medical research
• molecular medicine
• pathogenesis

• Humans
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/genetics
• Colitis, Ulcerative/metabolism
• Crohn Disease/diagnosis
• Crohn Disease/genetics
• Crohn Disease/metabolism
• Inflammatory Bowel Diseases
• Mucous Membrane/metabolism
• Receptors, Calcitriol/genetics

• Aage og Johanne Louis-Hansens Fond
• Herlev Hospital
• Colitis-Crohn Foreningen
• Torben og Alice Frimodts Fond
• Aase og Ejnar Danielsens Fond

• artificial neural network
• diagnostic model
• immune cell cells
• machine learning
• pediatric Crohn’s disease

Improved mucosal immune profiling in active and quiescent colonic inflammatory bowel disease (IBD) is needed to develop therapeutic options for treating and preventing flares. This study therefore aimed to provide a comprehensive mucosal characterization with emphasis on immunological host response of patients with active ulcerative colitis (UC active), UC during remission (UC remission) and active colonic Crohn’s disease (CD active).

Colonic biopsies from 47 study subjects were collected for gene expression and pathway analyses using the NanoString host-response panel, including 776 genes and 56 immune-related pathways.

The majority of mucosal gene expression and signaling pathway scores were increased in active IBD (n=27) compared to healthy subjects (n=10). However, both active IBD and UC remission (n=10) demonstrated decreased gene expression and signaling pathway scores related to autophagy, alpha kinase-1 and IL-17 signaling pathways compared to healthy subjects. Further, UC remission was characterized by decreased scores of several signaling pathways linked to homeostasis along with increased mononuclear cell migration pathway score as compared to healthy subjects. No major differences in the colonic mucosal gene expression between CD active (n=7) and UC (n=20) active were observed.

This study indicates that autophagy, alpha kinase-1 and IL-17 signaling pathways are persistently downregulated in UC irrespective of disease activity. Further, UC patients in remission present a unique mucosal environment, potentially preventing patients from reaching and sustaining true homeostasis. These findings may enable better comprehension of the remitting and relapsing pattern of colonic IBD and guide future treatment and prevention of flares.

• Swedish Foundation For Strategic Research
• Julins Foundation
• Bengt Ihre Fellowship
• Wilhelm and Martina Lundgren foundation
• the Mag-tarmfonden
• Svenska Läkarsällskapet
• the Calder foundation

• R01 DK099076 NIDDK NIH HHS

• inflammatory bowel disease
• intestinal epithelial barrier
• intestinal epithelial cells
• lncRNAs
• mRNAs

• Animals
• Colitis/chemically induced
• Colitis/genetics
• Dextran Sulfate
• Epithelial Cells/metabolism
• Gene Expression Profiling
• Gene Expression Regulation
• Gene Ontology
• Gene Regulatory Networks
• Intestines/cytology
• Male
• Mice, Inbred C57BL
• Molecular Sequence Annotation
• Protein Interaction Maps/genetics
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Reproducibility of Results
• Mice

• 2018LZXNYD-ZK19 Luzhou municipal people's government-southwest medical university science and technology strategic cooperation project
• Special Fund for High-level Talents (Chen Chen Team) of the People's Government of Luzhou-Southwestern Medical University
• 61427807 National Natural Science Foundation of China
• 81970468 National Natural Science Foundation of China
• Special Fund for High-level Talents (Shizhen Zhong Team) of the People's Government of Luzhou-Southwestern Medical University
• National Natural Science Foundation of China

• biomarker
• harmonization
• precision medicine
• prognosis
• treatment response

• Biomarkers/analysis
• Consensus
• Health Services Needs and Demand/trends
• Humans
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/therapy
• Outcome Assessment, Health Care/methods
• Prognosis
• Stakeholder Participation

• Crohn's and Colitis Foundation
• Biomarkers Consortium of the Foundation
• National Institutes of Health

• Crohn's disease
• imaging mass spectrometry
• inflammatory bowel disease
• ulcerative colitis

Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn's disease (CD), are chronic inflammatory disorders caused by genetic influences, the immune system and environmental factors. However, the underlying pathogenesis of IBDs and the pivotal molecular interactions remain to be fully elucidated. The aim of the present study was to identify genetic signatures in patients with IBDs and elucidate the potential molecular mechanisms underlying IBD subtypes. The gene expression profiles of the GSE75214 datasets were obtained from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified in UC and CD patients compared with controls using the GEO2R tool. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of DEGs were performed using DAVID. Furthermore, protein-protein interaction (PPI) networks of the DEGs were constructed using Cytoscape software. Subsequently, significant modules were selected and the hub genes were identified. In the GO and KEGG pathway analysis, the top enriched pathways in UC and CD included Staphylococcus aureus infection, rheumatoid arthritis, complement and coagulation cascades, PI3K/Akt signaling pathway and osteoclast differentiation. In addition, the GO terms in the category biological process significantly enriched by these genes were inflammatory response, immune response, leukocyte migration, cell adhesion, response to molecules of bacterial origin and extracellular matrix (ECM) organization. However, several other biological processes (GO terms) and pathways (e.g., ‘chemotaxis’, ‘collagen catabolic process’ and ‘ECM-receptor interaction’) exhibited significant differences between the two subtypes of IBD. The top 10 hub genes were identified from the PPI network using respective DEGs. Of note, the hub genes G protein subunit gamma 11 (GNG11), G protein subunit beta 4 (GNB4), Angiotensinogen (AGT), Phosphoinositide-3-kinase regulatory subunit 3 (PIK3R3) and C-C motif chemokine receptor 7 (CCR7) are disease-specific and may be used as biomarkers for differentiating UC from CD. Furthermore, module analysis further confirmed that common significant pathways involved in the pathogenesis of IBD subtypes were associated with chemokine-induced inflammation, innate immunity, adapted immunity and infectious microbes. In conclusion, the present study identified DEGs, key target genes, functional pathways and enrichment analysis of IBDs, enhancing the understanding of the pathogenesis of IBDs and also advancing the clarification of the underlying molecular mechanisms of UC and CD. Furthermore, these results may provide potential molecular targets and diagnostic biomarkers for UC and CD.

• Crohn's disease
• bioinformatics analysis
• differentially expressed genes
• hub genes
• inflammatory bowel disease
• module analysis
• protein-protein interaction network
• ulcerative colitis

• Proteomics
• differential expression analysis
• inflammatory bowel disease
• proteomic quantitative trait loci

• C-Reactive Protein/metabolism
• Case-Control Studies
• Colitis, Ulcerative/blood
• Colitis, Ulcerative/genetics
• Colitis, Ulcerative/metabolism
• Crohn Disease/blood
• Crohn Disease/genetics
• Crohn Disease/metabolism
• Databases, Genetic
• Humans
• Intestinal Mucosa/metabolism
• Proteome/genetics
• Proteome/metabolism
• Proteomics/methods
• RNA, Messenger/blood
• RNA, Messenger/metabolism
• Severity of Illness Index
• Transcriptome

• R01 DK092235 NIDDK NIH HHS
• S10 OD018522 NIH HHS
• U01 DK062422 NIDDK NIH HHS
• U24 DK062429 NIDDK NIH HHS

• IBD
• PTPN22
• genetics
• single nucleotide polymorphism
• ulcerative colitis

Inflammatory bowel disease (IBD) is a chronic intestinal disorder, with two main types: Crohn’s disease (CD) and ulcerative colitis (UC), whose molecular pathology is not well understood. The majority of IBD-associated SNPs are located in non-coding regions and are hard to characterize since regulatory regions in IBD are not known. Here we profile transcription start sites (TSSs) and enhancers in the descending colon of 94 IBD patients and controls. IBD-upregulated promoters and enhancers are highly enriched for IBD-associated SNPs and are bound by the same transcription factors. IBD-specific TSSs are associated to genes with roles in both inflammatory cascades and gut epithelia while TSSs distinguishing UC and CD are associated to gut epithelia functions. We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.

Many SNPs associated with inflammatory bowel disease are located in non-coding genomic regions. Here, the authors perform CAGE-sequencing on descending colon biopsies of Crohn’s disease and ulcerative colitis patients to map transcription start sites and enhancer activity for analysis of regulatory regions.

• Adult
• Child
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/drug therapy
• Crohn Disease/diagnosis
• Crohn Disease/drug therapy
• Humans
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/drug therapy
• Intestine, Small/pathology

Intestinal disorders often co-occur with inflammation and dysmotility. However, drugs which simultaneously improve intestinal inflammation and co-occurring dysmotility are rarely reported. Atractylodin, a widely used herbal medicine, is used to treat digestive disorders. The present study was designed to characterize the effects of atractylodin on amelioration of both jejunal inflammation and the co-occurring dysmotility in both constipation-prominent (CP) and diarrhea-prominent (DP) rats. The results indicated that atractylodin reduced proinflammatory cytokines TNF-α, IL-1β, and IL-6 in the plasma and inhibited the expression of inflammatory mediators iNOS and NF-kappa B in jejunal segments in both CP and DP rats. The results indicated that atractylodin exerted stimulatory effects and inhibitory effects on the contractility of jejunal segments isolated from CP and DP rats respectively, showing a contractile-state-dependent regulation. Atractylodin-induced contractile-state-dependent regulation was also observed by using rat jejunal segments in low and high contractile states respectively (5 pairs of low/high contractile states). Atractylodin up-regulated the decreased phosphorylation of 20 kDa myosin light chain, protein contents of myosin light chain kinase (MLCK), and MLCK mRNA expression in jejunal segments of CP rats and down-regulated those increased parameters in DP rats. Taken together, atractylodin alleviated rat jejunal inflammation and exerted contractile-state-dependent regulation on the contractility of jejunal segments isolated from CP and DP rats respectively, suggesting the potential clinical implication for ameliorating intestinal inflammation and co-occurring dysmotility.

• Atractylodin
• Constipation
• Contractile-state-dependent regulation
• Diarrhea
• Inflammation
• Jejunal contractility

Gastrointestinal symptoms are common in children with autism spectrum disorder (ASD). A significant proportion of children with ASD and gastrointestinal symptoms have histologic evidence of ileocolitis (inflammation of the terminal ileum and/or colon). We previously reported the molecular characterization of gastrointestinal biopsy tissue from ASD children with ileocolitis (ASD^IC+) compared to anatomically similar inflamed tissue from typically developing children with inflammatory bowel disease (IBD; i.e. Crohn’s disease or ulcerative colitis) and typically developing children with gastrointestinal symptoms but no evidence of gastrointestinal mucosal inflammation (TD^IC−). ASD^IC+ children had a gene expression profile that, while primarily overlapping with known IBD, had distinctive differences. The present study confirms these findings and replicates this molecular characterization in a second cohort of cases (ASD^IC+) and controls (TD^IC−). In these two separate case/control mucosal-based cohorts, we have demonstrated overlap of 59 differentially expressed transcripts (DETs) unique to inflamed ileocolonic tissue from symptomatic ASD^IC+ children. We now report that 9 of these 59 transcripts are also differentially expressed in the peripheral blood of the second cohort of ASD^IC+ children. This set of transcripts represents a putative blood-based biomarker for ASD-associated ileocolonic inflammation.

Irritable bowel syndrome (IBS), a common gastrointestinal disorder involving the gut-brain axis, and inflammatory bowel disease (IBD), a chronic relapsing inflammatory disorder, are both increasing in incidence and prevalence in Asia. Both have significant overlap in terms of symptoms, pathophysiology, and treatment, suggesting the possibility of IBS and IBD being a single disease entity albeit at opposite ends of the spectrum. We examined the similarities and differences in IBS and IBD, and offer new thoughts and approaches to the disease paradigm.

• Gut-brain axis
• IBS-IBD overlap syndrome
• Inflammatory bowel disease
• Irritable bowel syndrome

• fecal calprotectin
• immune activation
• inflammation
• inflammatory bowel disease
• irritable bowel syndrome
• remission

Ulcerative colitis (UC) is a relapsing and remitting disease with significant phenotypic and genotypic variability. Though more common in adults, UC is being increasingly diagnosed in childhood. The subsequent lifelong course of disease results in challenges for the patient and physician. Currently, there is no medical cure for UC. Even though surgical removal of the colon can be curative, complications including infertility in females make colectomy an option often considered only when the disease presents with life-threatening complications or when medical management fails. One of the greatest challenges the clinician faces in the care of patients with UC is the inability to predict at diagnosis which patient is going to respond to a specific therapy or will eventually require surgery. This therapeutic conundrum frames the discussion to follow, specifically the concept of individualized or personalized treatment strategies based on genetic risk factors. As we move to therapeutics, we will elucidate traditional approaches and discuss known and novel agents. As we look to the future, we can expect increasing integrated approaches using several scientific disciplines to inform how genetic interactions shape and mold the pathogenesis and therapeutics of UC.

• Ulcerative colitis
• genetic risk factors
• personalized treatment strategies
• therapeutics

There is currently no gold standard test for the diagnosis of inflammatory bowel disease (IBD). Physicians must rely on a number of diagnostic tools including clinical and endoscopic evaluation as well as histologic, serologic and radiologic assessment. The real difficulty for physicians in both primary and secondary care is differentiating between patients suffering from functional symptoms and those with true underlying IBD. Alongside this, there is always concern regarding the possibility of a missed, or delayed diagnosis of ulcerative colitis (UC) or Crohn’s disease. Even once the diagnosis of IBD has been made, there is often uncertainty in distinguishing between cases of UC or Crohn’s. As a consequence, in cases of incorrect diagnosis, optimal treatment and management may be adversely affected. Endoscopic evaluation can be uncomfortable and inconvenient for patients. It carries significant risks including perforation and in terms of monetary cost, is expensive. The use of biomarkers to help in the diagnosis and differentiation of IBD has been increasing over time. However, there is not yet one biomarker, which is sensitive of specific enough to be used alone in diagnosing IBD. Current serum testing includes C-reactive protein and erythrocyte sedimentation rate, which are cheap, reliable but non-specific and thus not ideal. Stool based testing such as faecal calprotectin is a much more specific tool and is currently in widespread clinical use. Non-invasive sampling is of the greatest clinical value and with the recent advances in metabolomics, genetics and proteomics, there are now more tools available to develop sensitive and specific biomarkers to diagnose and differentiate between IBD. Many of these new advances are only in early stages of development but show great promise for future clinical use.

• Biomarkers
• Inflammatory bowel disease
• Ulcerative colitis
• Crohn’s disease
• Indeterminate colitis

• Crohn’s disease
• biomarkers
• diagnosis
• differential diagnosis
• genetic testing
• inflammatory bowel disease
• serology

Distinction between Crohn’s disease of the colon-rectum and ulcerative colitis or inflammatory bowel disease (IBD) type unclassified can be of pivotal importance for a tailored clinical management, as each entity often involves specific therapeutic strategies and prognosis. Nonetheless, no gold standard is available and the uncertainty of diagnosis may frequently lead to misclassification or repeated examinations. Hence, we have performed a literature search to address the problem of differential diagnosis in IBD colitis, revised current and emerging diagnostic tools and refined disease classification strategies. Nowadays, the differential diagnosis is an untangled issue, and the proper diagnosis cannot be reached in up to 10% of patients presenting with IBD colitis. This topic is receiving emerging attention, as medical therapies, surgical approaches and leading prognostic outcomes require more and more disease-specific strategies in IBD patients. The optimization of standard diagnostic approaches based on clinical features, biomarkers, radiology, endoscopy and histopathology appears to provide only marginal benefits. Conversely, emerging diagnostic techniques in the field of gastrointestinal endoscopy, molecular pathology, genetics, epigenetics, metabolomics and proteomics have already shown promising results. Novel advanced endoscopic imaging techniques and biomarkers can shed new light for the differential diagnosis of IBD, better reflecting diverse disease behaviors based on specific pathogenic pathways.

• Crohn’s disease
• Ulcerative colitis
• Inflammatory bowel disease unclassified
• Advanced endoscopic imaging
• Biomarkers
• Histopathology

• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/therapy
• Crohn Disease/diagnosis
• Crohn Disease/therapy
• Diagnosis, Differential
• Diagnostic Techniques, Digestive System
• Humans
• Predictive Value of Tests
• Prognosis

• Diagnostic tool
• Dysbiosis
• Inflammatory bowel disease
• Metabolomics
• NMR spectroscopy

• Crohn's disease
• colonic mucosal biopsy
• diagnostics
• gene expression
• ulcerative colitis

• Animals
• Anion Transport Proteins/genetics
• Anion Transport Proteins/metabolism
• Anion Transport Proteins/physiology
• Arabidopsis
• Bicarbonates/metabolism
• Humans
• Mice
• Models, Biological
• Models, Molecular
• Multigene Family/genetics
• Mutation/genetics
• Phenotype
• Phylogeny
• Protein Conformation
• Protein Interaction Mapping
• Saccharomyces cerevisiae
• Species Specificity
• Sulfate Transporters

• P30 DK034854 NIDDK NIH HHS
• R37 DK043495 NIDDK NIH HHS
• DK34854 NIDDK NIH HHS
• DK43495 NIDDK NIH HHS

• Colonic biopsy
• Gene expression profiles
• Inflammatory bowel disease
• Metabolic profiles
• Metabolomics
• NMR spectroscopy

• G0802460 Medical Research Council

• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/pathology
• Disease Progression
• Disease-Free Survival
• Humans
• Models, Statistical
• Neoplasm Staging
• Recurrence
• Risk Assessment
• Survival Rate

• Child
• Child Development Disorders, Pervasive/complications
• Child Development Disorders, Pervasive/metabolism
• Child Development Disorders, Pervasive/pathology
• Child, Preschool
• Cohort Studies
• Colitis, Ulcerative/complications
• Colitis, Ulcerative/metabolism
• Colitis, Ulcerative/pathology
• Crohn Disease/complications
• Crohn Disease/metabolism
• Crohn Disease/pathology
• Female
• Gene Expression Profiling
• Gene Expression Regulation
• Humans
• Male
• Oligonucleotide Array Sequence Analysis
• Transcriptome

Irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) are chronic conditions affecting millions of individuals in the United States. The symptoms are well-documented and can be debilitating. How these chronic gastrointestinal (GI) conditions impact the daily lives of those afflicted is not well documented, especially from a patient's perspective.

Here we describe data from a series of 22 focus groups held at three different academic medical centers with individuals suffering from chronic GI conditions. All focus groups were audio recorded and transcribed. Two research team members independently analyzed transcripts from each focus group following an agreed upon coding scheme.

One-hundred-thirty-six individuals participated in our study, all with a chronic GI related condition. They candidly discussed three broad themes that characterize their daily lives: identification of disease and personal identity, medications and therapeutics, and daily adaptations. These all tie to our participants trying to deal with symptoms on a daily basis. We find that a recurrent topic underlying these themes is the dichotomy of experiencing uncertainty and striving for control.

Study participants' open dialogue and exchange of experiences living with a chronic GI condition provide insight into how these conditions shape day-to-day activities. Our findings provide fertile ground for discussions about how clinicians might best facilitate, acknowledge, and elicit patients' stories in routine care to better address their experience of illness.

• Adult
• Aged
• Biopsy
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/genetics
• Colitis, Ulcerative/pathology
• Crohn Disease/diagnosis
• Crohn Disease/genetics
• Crohn Disease/pathology
• Female
• Genetic Testing
• Genotype
• Humans
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/pathology
• Male
• Middle Aged
• Retrospective Studies
• Young Adult

• Crohn Disease/etiology
• Female
• Gastric Bypass/adverse effects
• Humans
• Middle Aged

• Adult
• Animals
• CD4-Positive T-Lymphocytes/immunology
• Cluster Analysis
• Colitis, Ulcerative/immunology
• Colitis, Ulcerative/parasitology
• Colitis, Ulcerative/pathology
• Colitis, Ulcerative/therapy
• Gene Expression Profiling
• Genetic Markers
• Humans
• Interleukins/immunology
• Intestinal Mucosa/parasitology
• Intestinal Mucosa/pathology
• Intestinal Mucosa/physiology
• Male
• Microarray Analysis
• Trichuriasis/immunology
• Trichuris/genetics
• Trichuris/pathogenicity
• Interleukin-22

• F32 AI066470 NIAID NIH HHS
• OD00329 NIH HHS

Ulcerative Colitis (UC) and Crohn's Disease (CD) are two chronic Inflammatory Bowel Diseases (IBD) affecting the intestinal mucosa. Current understanding of IBD pathogenesis points out the interplay of genetic events and environmental cues in the dysregulated immune response. We hypothesized that dysregulated microRNA (miRNA) expression may contribute to IBD pathogenesis. miRNAs are small, non-coding RNAs which prevent protein synthesis through translational suppression or mRNAs degradation, and regulate several physiological processes.

Expression of mature miRNAs was studied by Q-PCR in inactive colonic mucosa of patients with UC (8), CD (8) and expressed relative to that observed in healthy controls (10). Only miRNAs with highly altered expression (>5 or <0.2 -fold relative to control) were considered when Q-PCR data were analyzed. Two subsets of 14 (UC) and 23 (CD) miRNAs with highly altered expression (5.2->100 -fold and 0.05–0.19 -fold for over- and under- expression, respectively; 0.001<p≤0.05) were identified in quiescent colonic mucosa, 8 being commonly dysregulated in non-inflamed UC and CD (mir-26a,-29a,-29b,-30c,-126*,-127-3p,-196a,-324-3p). Several miRNA genes with dysregulated expression co-localize with acknowledged IBD-susceptibility loci while others, (eg. clustered on 14q32.31), map on chromosomal regions not previously recognized as IBD-susceptibility loci. In addition, in silico clustering analysis identified 5 miRNAs (mir-26a,-29b,-126*,-127-3p,-324-3p) that share coordinated dysregulation of expression both in quiescent and in inflamed colonic mucosa of IBD patients. Six miRNAs displayed significantly distinct alteration of expression in non-inflamed colonic biopsies of UC and CD patients (mir-196b,-199a-3p,-199b-5p,-320a,-150,-223).

Our study supports miRNAs as crucial players in the onset and/or relapse of inflammation from quiescent mucosal tissues in IBD patients. It allows speculating a role for miRNAs as contributors to IBD susceptibility and suggests that some of the miRNA with altered expression in the quiescent mucosa of IBD patients may define miRNA signatures for UC and CD and help develop new diagnostic biomarkers.

• Chromosome Mapping
• Colon/metabolism
• Female
• Humans
• Inflammatory Bowel Diseases/metabolism
• Intestinal Mucosa/metabolism
• Male
• MicroRNAs/genetics
• Polymerase Chain Reaction

• chondrodysplasia
• nephrolithiasis
• oxalosis
• anion exchange
• xenopus oocyte

• Animals
• Anion Transport Proteins/genetics
• Anion Transport Proteins/metabolism
• Biological Transport
• Cell Membrane/drug effects
• Cell Membrane/metabolism
• Humans
• Hydrogen-Ion Concentration
• Kinetics
• Mice
• Mutation
• Oocytes
• Oxalic Acid/metabolism
• Protein Kinase C/antagonists & inhibitors
• Protein Kinase C/metabolism
• Protein Kinase Inhibitors/pharmacology
• Sodium Chloride/metabolism
• Sulfate Transporters
• Sulfates/metabolism
• Xenopus