IL-17a and IL-22 Induce Expression of Antimicrobials in Gastrointestinal Epithelial Cells and May Contribute to Epithelial Cell Defense against Helicobacter pylori
| العنوان: | IL-17a and IL-22 Induce Expression of Antimicrobials in Gastrointestinal Epithelial Cells and May Contribute to Epithelial Cell Defense against Helicobacter pylori |
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| المؤلفون: | Jana N. Radin, Beverly R. E. A. Dixon, Diana C. Contreras, Holly M. Scott Algood, M. Blanca Piazuelo |
| المصدر: | PLoS ONE PLoS ONE, Vol 11, Iss 2, p e0148514 (2016) |
| سنة النشر: | 2015 |
| مصطلحات موضوعية: | 0301 basic medicine, CD4-Positive T-Lymphocytes, Male, Chemokine, Physiology, lcsh:Medicine, Pathology and Laboratory Medicine, Epithelium, Interleukin 22, Mice, 0302 clinical medicine, Anti-Infective Agents, Animal Cells, Helicobacter, Immune Physiology, Medicine and Health Sciences, Gastrointestinal Infections, lcsh:Science, Immune Response, Innate Immune System, Multidisciplinary, biology, Antimicrobials, Interleukin-17, Stomach, Drugs, Animal Models, Lipocalins, 3. Good health, Bacterial Pathogens, medicine.anatomical_structure, Medical Microbiology, Gastritis, Cytokines, Interleukin 17, medicine.symptom, Pathogens, Cellular Types, Anatomy, Research Article, T cell, Immunology, Inflammation, Mice, Transgenic, Mouse Models, Gastroenterology and Hepatology, Real-Time Polymerase Chain Reaction, Research and Analysis Methods, Microbiology, Helicobacter Infections, 03 medical and health sciences, Immune system, Model Organisms, Signs and Symptoms, Microbial Control, medicine, Animals, Humans, Microbial Pathogens, Pharmacology, Helicobacter pylori, Bacteria, Interleukins, lcsh:R, Interleukin-8, Organisms, Biology and Life Sciences, Epithelial Cells, Cell Biology, Molecular Development, biology.organism_classification, Gastrointestinal Tract, Mice, Inbred C57BL, 030104 developmental biology, Biological Tissue, Immune System, biology.protein, lcsh:Q, Leukocyte L1 Antigen Complex, Digestive System, 030215 immunology, Developmental Biology |
| الوصف: | Helicobacter pylori colonization of the human stomach can lead to adverse clinical outcomes including gastritis, peptic ulcers, or gastric cancer. Current data suggest that in addition to bacterial virulence factors, the magnitude and types of immune responses influence the outcome of colonization. Specifically, CD4+ T cell responses impact the pathology elicited in response to H. pylori. Because gastritis is believed to be the initiating host response to more detrimental pathological outcomes, there has been a significant interest in pro-inflammatory T cell cytokines, including the cytokines produced by T helper 17 cells. Th17 cells produce IL-17A, IL-17F, IL-21 and IL-22. While these cytokines have been linked to inflammation, IL-17A and IL-22 are also associated with anti-microbial responses and control of bacterial colonization. The goal of this research was to determine the role of IL-22 in activation of antimicrobial responses in models of H. pylori infection using human gastric epithelial cell lines and the mouse model of H. pylori infection. Our data indicate that IL-17A and IL-22 work synergistically to induce antimicrobials and chemokines such as IL-8, components of calprotectin (CP), lipocalin (LCN) and some β-defensins in both human and primary mouse gastric epithelial cells (GEC) and gastroids. Moreover, IL-22 and IL-17A-activated GECs were capable of inhibiting growth of H. pylori in vitro. While antimicrobials were activated by IL-17A and IL-22 in vitro, using a mouse model of H. pylori infection, the data herein indicate that IL-22 deficiency alone does not render mice more susceptible to infection, change their antimicrobial gene transcription, or significantly change their inflammatory response. |
| تدمد: | 1932-6203 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d8add4d161bed1e409340d4a45a93c27 https://pubmed.ncbi.nlm.nih.gov/26867135 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....d8add4d161bed1e409340d4a45a93c27 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19326203 |
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