• Autoimmune diseases
• IL-1R2
• Immune cells
• Immune disorders

• Humans
• Receptors, Interleukin-1 Type II/metabolism
• Receptors, Interleukin-1 Type II/genetics
• Autoimmune Diseases/immunology
• Animals

• Caco-2
• IL-1R
• IL-1β
• geraniin
• inflammatory bowel disease
• intestinal barrier function

• Humans
• Animals
• Mice
• Caco-2 Cells
• Dextran Sulfate/adverse effects
• Dextran Sulfate/metabolism
• NF-kappa B/genetics
• NF-kappa B/metabolism
• Colitis/chemically induced
• Colitis/drug therapy
• Colitis/genetics
• Inflammation/metabolism
• Inflammatory Bowel Diseases/chemically induced
• Inflammatory Bowel Diseases/drug therapy
• Inflammatory Bowel Diseases/metabolism
• Mice, Inbred C57BL
• Disease Models, Animal
• Intestinal Mucosa/metabolism
• Glucosides
• Hydrolyzable Tannins

• CP: Immunology
• IL-1β
• Nr4a1
• T cell receptor signaling
• Treg cells
• inflammatory bowel diseases
• naive CD4(+) T cells

• Humans
• Mice
• Animals
• CD4-Positive T-Lymphocytes
• T-Lymphocytes, Regulatory
• Cell Differentiation
• Receptors, Antigen, T-Cell
• Colitis

• LRRK2 G2019S
• colitis
• colon cancer
• inflammation

• Animals
• Mice
• Colitis/chemically induced
• Colitis/complications
• Colitis/genetics
• Colonic Neoplasms/genetics
• Gasdermins
• Inflammation/genetics
• Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics
• Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/metabolism
• Tumor Microenvironment

• R01 NS104164 NIH HHS
• R01 AI155425 NIAID NIH HHS
• R21 NS130559 NINDS NIH HHS
• R01 NS104164 NINDS NIH HHS
• R21AG076895 NIH HHS

• IL-18
• IL-1β
• Inflammatory bowel diseases
• NLRP3 inflammasome
• fibroblasts
• fibrosis
• mucosal immune system
• small molecule inhibitor

• Humans
• NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
• Inflammasomes/metabolism
• Inflammatory Bowel Diseases
• Mucous Membrane/metabolism
• Interleukin-1beta/metabolism
• Inflammation
• Fibroblasts/metabolism
• Collagen
• Fibrosis

• 101080523 European Union Agency for Network and Information Security
• European Health and Digital Executive Agency
• Deutsche Forschungsgemeinschaft

• Dextran Sodium Sulfate (DSS)
• colitis
• gut microbiota
• inflammatory bowel disease (IBD)
• red cabbage
• short-chain fatty acids (SCFAs)

• Animals
• Mice
• Mice, Inbred C57BL
• Gastrointestinal Microbiome
• Colitis/chemically induced
• Inflammatory Bowel Diseases
• Homeostasis

• R01 CA247763 NCI NIH HHS

• diet
• food allergy
• formula
• immune system
• inflammation
• necrotizing enterocolitis
• neonatal intensive care unit
• premature infant

• KL2 TR001452 NCATS NIH HHS
• P30 DK123704 NIDDK NIH HHS
• UL1 TR001450 NCATS NIH HHS

• anti-inflammatory effect
• gut microbiota
• short-chain fatty acids
• tamarind seed polysaccharide hydrolysate
• ulcerative colitis

• Flavonoids
• Inflammatory bowel disease
• Microencapsulated delivery system
• Nuclear factor-κB
• Oxidative stress

• Mice
• Animals
• Chalcones
• Caseins
• Chalcone/pharmacology
• Capsules/pharmacology
• Pectins
• Colitis/chemically induced
• Colitis/drug therapy
• Colon
• NF-kappa B
• Disease Models, Animal

• R01 AI155425 NIAID NIH HHS
• R01 NS104164 NINDS NIH HHS
• R21 NS130559 NINDS NIH HHS

• Animals
• Mice
• Non-alcoholic Fatty Liver Disease/metabolism
• Microplastics
• Polystyrenes/toxicity
• Plastics/metabolism
• Diet, High-Fat/adverse effects
• Liver/metabolism
• Inflammation
• Glucose/metabolism
• Mice, Inbred C57BL

• Allium sativum
• aged garlic extract
• allicin
• cytokines
• diseases
• health benefits
• inflammatory bowel disease
• organosulfur compounds

• KATP channels
• cGMP
• cyclic guanosine monophosphate
• inflammatory bowel disease
• montelucast
• nitric oxide
• rats

• Colitis
• Dextran sulfate sodium
• Inflammasomes
• Inflammatory bowel diseases
• NLRP3

• Colitis
• HSP90 inhibitor
• Inflammasome
• NLRP3 autophagic degradation
• TAS-116/metformin

Inflammatory bowel disease (IBD) has been reported to be associated with NLRP3 inflammasome activation. Therefore inhibiting inflammasome activation could be a new approach to treat IBD. Inflammasome inhibitors NLRP3-IN-2, JC124, and 3,4-methylenedioxy-β-nitrostyrene (MNS) were previously reported to exert anti-inflammatory effects in various disease models but not in the dextran sulfate sodium (DSS)–induced colitis model. Here, we showed that MNS was more efficient in inhibiting the secretion of interleukin-1β (IL-1β) by blocking oligomerization of apoptosis-associated speck-like protein (ASC) than NLRP3-IN-2 and JC124. To investigate the protective effects of MNS on enteritis, we administered intragastric MNS to DSS-induced colitis mice. The results demonstrated that MNS attenuated DSS-induced body weight loss, colon length shortening, and pathological damage. In addition, MNS inhibited the infiltration of macrophages and inflammatory cells and reduced IL-1β and IL-12p40 pro-inflammatory cytokines but had no significant effect on tumor necrosis factor α (TNF-α) and IL-6. Furthermore, we also found that the differentiation of IL-17A⁺interferon-γ (IFN-γ)⁺CD4⁺ T cell was decreased in the colon after MNS treatment, which might be mediated by IL-1β, etc. cytokine release. Taken together, MNS alleviated DSS-induced intestinal inflammation by inhibiting NLRP3 inflammasome activation, which may function as an effective therapeutic for IBD.

• Natural Science Foundation of Shandong Province
• Qingdao Postdoctoral Science Foundation
• National Natural Science Foundation of China

• Claudin
• Genetics
• IL23
• JAK-STAT
• MLCK
• TNF
• Tight Junction
• Toll-Like Receptor

• Creeping fat
• Crohn’s disease
• microbiota

• Drug delivery systems
• Inflammatory bowel disease
• Nanoparticles
• Polysaccharides

• Administration, Oral
• Drug Delivery Systems/methods
• Gastrointestinal Agents/administration & dosage
• Gastrointestinal Agents/adverse effects
• Gastrointestinal Agents/therapeutic use
• Humans
• Hydrogen-Ion Concentration
• Inflammation Mediators/physiology
• Inflammatory Bowel Diseases/drug therapy
• Inflammatory Bowel Diseases/physiopathology
• Mucus/metabolism
• Nanoparticle Drug Delivery System/pharmacology
• Polysaccharides/administration & dosage
• Polysaccharides/pharmacology

This study aimed to evaluate the benefits of oral administration of Lactobacillus acidophilus strain L-55 (LaL-55) to chickens inoculated with a Newcastle disease virus (NDV)-based live-attenuated vaccine by examining the mRNA expression of several genes related to viral infection in the spleen and ileum by quantitative reverse transcription polymerase chain reaction. In the spleen, interferon (IFN)-α was significantly higher in the low- and middle-dose LaL-55 groups at 6 weeks than at 4 weeks. IFN regulatory factor (IRF)-3 and IRF-7 expression was significantly higher in the low-dose LaL-55 group than in the middle- and high-dose LaL-55 groups. In the ileum, melanoma differentiation-associated gene 5 showed a dose-dependent increase at 4 weeks. IFN-γ and IRF-7 showed dose-dependent increases at 6 weeks. These results suggested that LaL-55 boosts the immune response to the NDV vaccine, albeit by different mechanisms in the spleen and ileum.

Salmonella infection remains one of the major public health problems in the world, with increasing resistance to antibiotics. The resolution is to explore the pathogenesis of the infection and search for alternative therapy other than antibiotics. Immune responses to Salmonella infection include innate and adaptive immunity. Flagellin or muramyl dipeptide from Salmonella, recognized by extracellular Toll-like receptors and intracellular nucleotide-binding oligomerization domain2, respectively, induce innate immunity involving intestinal epithelial cells, neutrophils, macrophages, dendric cells and lymphocytes, including natural killer (NK) and natural killer T (NKT) cells. The cytokines, mostly interleukins, produced by the cells involved in innate immunity, stimulate adaptive immunity involving T and B cells. The mucosal epithelium responds to intestinal pathogens through its secretion of inflammatory cytokines, chemokines, and antimicrobial peptides. Chemokines, such as IL-8 and IL-17, recruit neutrophils into the cecal mucosa to defend against the invasion of Salmonella, but induce excessive inflammation contributing to colitis. Some of the interleukins have anti-inflammatory effects, such as IL-10, while others have pro-inflammatory effects, such as IL-1β, IL-12/IL-23, IL-15, IL-18, and IL-22. Furthermore, some interleukins, such as IL-6 and IL-27, exhibit both pro- and anti-inflammatory functions and anti-microbial defenses. The majority of interleukins secreted by macrophages and lymphocytes contributes antimicrobial defense or protective effects, but IL-8 and IL-10 may promote systemic Salmonella infection. In this article, we review the interleukins involved in Salmonella infection in the literature.

• Salmonella
• immune response
• interleukin
• intestine
• mucosa

• Animals
• Humans
• Immunity
• Immunity, Mucosal
• Interleukins/metabolism
• Intestines/immunology
• Intestines/microbiology
• Salmonella Infections/immunology
• Salmonella Infections/microbiology

• NF-kappaB (NF-κB)
• interleukin-1β (IL-1β)
• intestinal inflammation
• intestinal tight junction (TJ) barrier
• microRNA
• myosin light chain kinase (MLCK)

• Acetic acid-induced colitis
• Canagliflozin
• Inflammatory response
• NOX2
• Oxidative stress
• SGLT-2

• Acetic Acid
• Animals
• Antioxidants/metabolism
• Canagliflozin/therapeutic use
• Colitis/chemically induced
• Colitis/drug therapy
• Colitis/metabolism
• Colon/pathology
• Glucose/metabolism
• Male
• NADPH Oxidase 2/metabolism
• Organ Size
• Oxidative Stress/drug effects
• Rats
• Rats, Wistar
• Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
• Sulfasalazine/therapeutic use

• Colitis
• Gracilaria lemaneiformis polysaccharide
• Gut microbiota
• Intestinal barrier
• Short chain fatty acid

The rs315952 (Ser133Ser) has been reported to influence the risk for immune-mediated as well as inflammatory diseases in many studies; however, the results remain inconsistent. The current meta-analysis was performed to give a more precise estimation for the relationship between this IL-1Ra missense variant and the risk of both types of diseases.

Relevant publications were retrieved through a literature search in Web of Science, Medline, PubMed, Scopus, EMBASE, and Google scholar search engines, between 2000 and 2019. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the strength of the association.

Twenty-two studies, including 2622 cases with and 3854 controls were identified. The IL-1Ra Ser133Ser variant does not confer an increased overall risk for immune-mediated and inflammatory diseases. This variant was statistically associated with decreased risk of systemic lupus erythematosus (under allelic, codominant heterozygous, and dominant models) or ankylosing spondylitis (in allelic and recessive models)(OR<1). Moreover, alleles, as well as genotypes of the IL-1Ra Ser133Ser variant, may confer an increased risk of immune-mediated and inflammatory diseases in Hispanics. However, this variant was not associated with susceptibility to immune-mediated and inflammatory diseases in both Asians and Arabs.

The pooled results fail to support the hypothesis that the IL-1Ra Ser133Ser variant is associated with the overall risk of immune-mediated and inflammatory diseases. Performing large scale replication and meta-analysis of functional variants within this gene is encouraged to further investigate the influence of IL-1Ra SNPs on overall disease susceptibility.

• Autoimmunity
• Inflammation
• Meta-analysis
• Polymorphism

• Hesperidin methyl chalcone
• Inflammation
• Oxidative stress
• Ulcerative colitis

The increased incidence of inflammatory bowel disease (IBD) in Western and rapidly Westernizing developing countries poses a global pandemic threat. The development of affordable drugs for treating IBD worldwide is thus a priority. Genetically modified lactic acid bacteria (gmLAB) as microbial therapeutics are inexpensive protein producers suitable for use as carriers of protein to the intestinal mucosa. Here, we successfully constructed gmLAB hypersecreting interleukin 1 receptor antagonist (IL-1Ra). Oral administration of these gmLAB suppressed body weight reduction and exacerbation of the disease activity index score in mice with acute colitis and decreased the number of CD4⁺ IL-17A⁺ cells in the mesenteric lymph nodes. These data suggest that the gmLAB deliver IL-1Ra to the colon, where it inhibits IL-1 signaling. We thus developed a novel IBD therapeutic that blocks IL-1 signaling using a gmLAB protein delivery system. This system could be an inexpensive oral microbial therapeutic.

Genetically reprogrammed bacteria can facilitate the efficient delivery of a therapeutic protein for treating inflammatory bowel disease (IBD). Interleukin 1 receptor antagonist (IL-1Ra) inhibits the immune cells that attack the intestinal lining in IBD patients, but current administration strategies are associated with serious side effects. Takeshi Shimosato and colleagues at Shinshu University in Nagano, Japan, have engineered the microbe Lactococcus lactis to secrete high levels of IL-1Ra. The researchers dosed mice orally with these bacteria, which released IL-1Ra into the intestinal tissue. This treatment proved safe and effectively reduced inflammation and associated symptoms in a mouse model of ulcerative colitis. L. lactis has previously been tested as a probiotic in clinical trials, and may therefore offer an appealing alternative to subcutaneous administration of IBD drugs in human patients.

Antibiotics and pharmacological zinc supplementation were commonly used as growth promoters for several decades in the swine industry before being limited because of public health and environmental concerns. Further, the physiological and metabolic responses associated with their growth promotion effects are unclear. To characterize these responses induced by pharmacological zinc supplementation (2500 mg/kg) and carbadox (55 mg/kg), 192 post-weaning pigs were fed basal and test diets for 43 days. Compared with basal, pharmacological zinc and carbadox independently improved growth performance. Pharmacological zinc increased gastric mucosa thickness compared with basal zinc, while carbadox increased intestinal villus:crypt ratio compared with non-carbadox. Pharmacological zinc and carbadox independently reduced interleukin (IL)-1β concentration compared with basal zinc and non-carbadox. Pharmacological zinc increased IL-1RA:IL-1 ratio by 42% compared with basal zinc, while carbadox tended to increase the IL-10 and IL10:IL-12 ratio compared with non-carbadox. Carbadox increased fecal concentrations of histidine and lysine compared with non-carbadox. The independent effect of pharmacological zinc and carbadox on morphology and nutrient metabolism, and their shared effect on immunity may contribute to the additive effect on growth promotion. These results further confirmed the concept that growth promotion is multifactorial intervention. Therefore, elucidating growth-promoting effects and searching for alternatives should include wide-spectrum evaluation.

• animal production
• carbadox
• cytokines
• gastrointestinal tract
• gut metabolites
• zinc oxide

• ERK2
• HCV
• IFN-α
• IL-1β
• ISG
• STAT1

• Colitis
• De-epoxy-DON: DOM-1
• Immune response
• Intestine
• Mycotoxin
• Spleen

• Ginsenosides Rk3
• Inflammation
• NLRP3
• Short-chain fatty acids
• Tight junctions
• Ulcerative colitis

Inflammatory bowel diseases (IBD) are the most common gastrointestinal inflammatory pathologies. Previous work evidenced a lower content of nicotinic acid (NA) in feces of IBD patients compared to healthy subjects. In the present study, we aimed to understand the effects of NA on intestinal inflammation, as several studies reported its possible beneficial effect, and investigate its influence on inflammation-driven metabolism. NA was tested on a Caco-2 in-vitro model in which inflammation was induced with interleukin-1β (IL-1β) and lipopolysaccharide (LPS), two mayor proinflammatory compounds produced in IBD, that stimulate the production of cytokines, such as interleukin 8. A metabolomics approach, with gas chromatography–mass spectrometry (GC-MS) and nuclear proton magnetic resonance (¹H-NMR), was applied to study the metabolic changes. The results showed that NA significantly reduced the level of IL-8 produced in both LPS and IL-1β stimulated cells, confirming the anti-inflammatory effect of NA also on intestinal inflammation. Moreover, it was demonstrated that NA treatment had a restoring effect on several metabolites whose levels were modified by treatments with IL-1β or LPS. This study points out a possible use of NA as anti-inflammatory compound and might be considered as a promising starting point in understanding the beneficial effect of NA in IBD.

• IBD
• inflammation
• metabolomics
• nicotinic acid

Nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a cell-surface adhesion molecule that regulates cell migration and attachment. This study demonstrates the increase in Ninj1 protein expression during development of intestinal inflammation. Ninj1-deficient mice exhibited significantly attenuated bodyweight loss, shortening of colon length, intestinal inflammation, and lesser pathological lesions than wild-type mice. Although more severe inflammation and serious lesions are observed in wild-type mice than Ninj1-deficient mice, there were no changes in the numbers of infiltrating macrophages in the inflamed tissues obtained from WT and Ninj1-deficient mice. Ninj1 expression results in activation of macrophages, and these activated macrophages secrete more cytokines and chemokines than Ninj1-deficient macrophages. Moreover, mice with conditional deletion of Ninj1 in myeloid cells (Ninj1^fl/fl; Lyz-Cre+) alleviated experimental colitis compared with wild-type mice. In summary, we propose that the Ninj1 in myeloid cells play a pivotal function in intestinal inflammatory conditions.

• IBD
• IL1β
• Ninjurin1
• inflammation
• myeloid cells

• Animals
• Cell Adhesion
• Cell Adhesion Molecules, Neuronal/physiology
• Cell Movement
• Cells, Cultured
• Colitis/etiology
• Colitis/metabolism
• Colitis/pathology
• Colitis/prevention & control
• Female
• Inflammation/etiology
• Inflammation/metabolism
• Inflammation/pathology
• Inflammation/prevention & control
• Intestinal Diseases/etiology
• Intestinal Diseases/metabolism
• Intestinal Diseases/pathology
• Intestinal Diseases/prevention & control
• Male
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Myeloid Cells/metabolism
• Nerve Growth Factors/physiology
• Signal Transduction

• IL-1Ra deficient
• inflammatory bowel disease
• intestinal enzymes
• matrix-degrading enzymes
• pro-inflammatory cytokines

• abdominal pain
• inflammation
• inflammatory bowel syndrome
• inflammatory pain
• oxidative stress

The chronic inflammatory process underlying inflammatory bowel disease (IBD), comprising Crohn’s disease and ulcerative colitis, derives from the interplay of several components in a genetically susceptible host. These components include environmental elements and gut microbiota a dysbiosis. For decades, immune abnormalities have been investigated as critically important in IBD pathogenesis, and attempts to develop effective therapies have predominantly targeted the immune system. Nevertheless, immune events represent only one of the constituents contributing to IBD pathogenesis within the context of the complex cellular and molecular network underlying chronic intestinal inflammation. These factors need to be appreciated within the milieu of non-immune components. Damage-associated molecular patterns (DAMPs), which are essentially endogenous stress proteins expressed or released as a result of cell or tissue damage, have been shown to act as direct pro-inflammatory mediators. Excessive or persistent signalling mediated by such molecules can underlie several chronic inflammatory disorders, including IBD. The release of endogenous DAMPs amplifies the inflammatory response driven by immune and non-immune cells and promotes epigenetic reprogramming in IBD. The effects determine pathologic changes, which may sustain chronic intestinal inflammation and also underlie specific disease phenotypes. In addition to highlighting the potential use of DAMPs such as calprotectin as biomarkers, research on DAMPs may reveal novel mechanistic associations in IBD pathogenesis and is expected to uncover putative therapeutic targets.

• Damage-associated molecular patterns
• Environmental factors
• Epigenetics
• Inflammatory bowel disease
• Therapeutic targets

• Biomarkers/analysis
• Biomarkers/metabolism
• Cellular Reprogramming/genetics
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/immunology
• Colitis, Ulcerative/microbiology
• Colitis, Ulcerative/pathology
• Crohn Disease/drug therapy
• Crohn Disease/immunology
• Crohn Disease/microbiology
• Crohn Disease/pathology
• Dysbiosis/genetics
• Dysbiosis/immunology
• Dysbiosis/microbiology
• Dysbiosis/pathology
• Epigenesis, Genetic
• Gastrointestinal Agents/pharmacology
• Gastrointestinal Agents/therapeutic use
• Gastrointestinal Microbiome/immunology
• Genetic Predisposition to Disease
• Humans
• Inflammation Mediators/analysis
• Inflammation Mediators/antagonists & inhibitors
• Inflammation Mediators/metabolism
• Intestinal Mucosa/cytology
• Intestinal Mucosa/immunology
• Intestinal Mucosa/microbiology
• Intestinal Mucosa/pathology
• Leukocyte L1 Antigen Complex/analysis
• Leukocyte L1 Antigen Complex/metabolism
• Molecular Targeted Therapy/methods

• Curcumin
• Dextran sulfate sodium
• IL-1β
• Inflammatory bowel diseases
• NLRP3 inflammasome

Homeostasis at mucosal surfaces requires cross-talk between the environment and barrier epithelial cells. Disruption of barrier function typifies mucosal disease. Here we elucidate a bifunctional role in coordinating this cross-talk for the inflammatory bowel disease risk-gene INAVA. Both activities require INAVA’s DUF3338 domain (renamed CUPID). CUPID stably binds the cytohesin ARF-GEF ARNO to effect lateral membrane F-actin assembly underlying cell-cell junctions and barrier function. Unexpectedly, when bound to CUPID, ARNO affects F-actin dynamics in the absence of its canonical activity as a guanine nucleotide-exchange factor. Upon exposure to IL-1β, INAVA relocates to form cytosolic puncta, where CUPID amplifies TRAF6-dependent polyubiquitination and inflammatory signaling. In this case, ARNO binding to CUPID negatively-regulates polyubiquitination and the inflammatory response. INAVA and ARNO act similarly in primary human macrophages responding to IL-1β and to NOD2 agonists. Thus, INAVA-CUPID exhibits dual functions, coordinated directly by ARNO, that bridge epithelial barrier function with extracellular signals and inflammation.

• ARNO
• IL-1b
• TRAF6
• actin assembly
• biochemistry
• cell biology
• chemical biology
• epithelial barrier
• human
• inflammatory bowel disease

To explore the effects of abdominal surgery and interleukin-1 signaling on antimicrobial defense in a model of postoperative ileus.

C57BL/6 and Interleukin-1 receptor type I (IL-1R1) deficient mice underwent intestinal manipulation to induce POI. Expression of mucosal IL-1α, IL-1β and IL-1R1 and several antimicrobial peptides and enzymes were measured by quantitative PCR or ELISA, western blotting or immunohistochemistry. Bacterial overgrowth was determined by fluorescent in-situ hybridization and counting of jejunal luminal bacteria. Translocation of aerobic and anaerobic bacteria into the intestinal wall, mesenteric lymph nodes, liver and spleen was determined by counting bacterial colonies on agar plates 48h after plating of tissue homogenates. Antimicrobial activity against E. coli and B. vulgatus was analyzed in total and cationic fractions of small bowel mucosal tissue homogenates by a flow cytometry-based bacterial depolarization assay.

Jejunal bacterial overgrowth was detected 24h after surgery. At the same time point, but not in the early phase 3h after surgery, bacterial translocation into the liver and mesenteric lymph nodes was observed. Increased antimicrobial activity against E. coli was induced within early phase of POI. Basal antimicrobial peptide and enzyme gene expression was higher in the ileal compared to the jejunal mucosa. The expression of lysozyme 1, cryptdin 1, cryptdin 4 and mucin 2 were reduced 24h after surgery in the ileal mucosa and mucin 2 was also reduced in the jejunum. Postoperative IL-1α and IL-1β were increased in the postoperative mucosa. Deficiency of IL-1R1 affected the expression of antimicrobial peptides during homeostasis and POI.

Small bowel antimicrobial capacity is disturbed during POI which is accompanied by bacterial overgrowth and translocation. IL-1R1 is partially involved in the gene expression of mucosal antimicrobial peptides. Altered small bowel antimicrobial activity may contribute also to POI development and manifestation in patients undergoing abdominal surgery.

• Animals
• Disease Models, Animal
• Ileus/metabolism
• Ileus/microbiology
• Ileus/pathology
• Intestinal Mucosa/metabolism
• Intestinal Mucosa/microbiology
• Intestinal Mucosa/pathology
• Male
• Mice
• Postoperative Complications/metabolism
• Postoperative Complications/microbiology
• Postoperative Complications/pathology
• Receptors, Interleukin-1 Type I/metabolism
• Signal Transduction

• BONFOR

• Dendritic cells
• Gastroenterology
• Immunology
• Inflammatory bowel disease
• T cells