Extracellular Signal-Regulated Protein Kinase Mediates Interleukin 17 (IL-17)-Induced IL-8 Secretion in Helicobacter pylori-Infected Human Gastric Epithelial Cells

التفاصيل البيبلوغرافية
العنوان: Extracellular Signal-Regulated Protein Kinase Mediates Interleukin 17 (IL-17)-Induced IL-8 Secretion in Helicobacter pylori-Infected Human Gastric Epithelial Cells
المؤلفون: Antonia Pellicanò, Giovanni Monteleone, Francesco Pallone, Francesco Luzza, Maria Imeneo, Ladislava Sebkova, Barbara Grazioli, G. Guarnieri
المصدر: Infection and Immunity. 82:2158-2158
بيانات النشر: American Society for Microbiology, 2014.
سنة النشر: 2014
مصطلحات موضوعية: MAPK/ERK pathway, Male, mitogen activated protein kinase inhibitor, bacterial colonization, Mitogen-Activated Protein Kinase 3, stomach biopsy, Western blotting, immunoglobulin G, Cells, Cultured, Mitogen-Activated Protein Kinase 1, Settore MED/12 - Gastroenterologia, Host Response and Inflammation, Cultured, biology, mitogen activated protein kinase, Kinase, Interleukin-17, transcription factor AP 1, article, neutralizing antibody, nuclear factor, Middle Aged, immunoglobulin enhancer binding protein, medicine.anatomical_structure, Infectious Diseases, cytokine release, priority journal, Mitogen-activated protein kinase, cytokine production, mucosa inflammation, Female, Interleukin 17, CagA protein, Mitogen-Activated Protein Kinases, signal transduction, Adult, Cells, Immunology, cell stimulation, interleukin 6, interleukin 8, gel mobility shift assay, Microbiology, Helicobacter infection, Cell Line, Helicobacter Infections, reverse transcription polymerase chain reaction, Gastric mucosa, medicine, CagA, Humans, controlled study, Secretion, human, Interleukin 8, Author Correction, Protein kinase A, Aged, nonhuman, Helicobacter pylori, human cell, Interleukin-8, Epithelial Cells, biology.organism_classification, Molecular biology, human tissue, enzyme linked immunosorbent assay, Enzyme Activation, mitogen activated protein kinase 1, Gene Expression Regulation, Extracellular signal, Gastric Mucosa, biology.protein, Parasitology, stomach epithelium, interleukin 17, enzyme activation
الوصف: Helicobacter pylori -induced mucosal inflammation results in high production of interleukin 17 (IL-17), a potent inducer of IL-8 in gastric epithelial cells. The aim of this study was to investigate signaling pathways by which IL-17 regulates IL-8 production in human gastric epithelial cells. Activation of mitogen-activated protein (MAP) kinases in both IL-17-stimulated MKN28 cells and epithelial cells isolated from H. pylori -colonized gastric mucosa was assessed by Western blotting. In IL-17-stimulated MKN28 cells the activation of activatior protein 1 (AP-1), nuclear factor (NF)-IL-6, and NF-κB was also assessed by electrophoretic mobility shift assay. IL-8 production was evaluated by reverse transcription-PCR and enzyme-linked immunosorbent assay (ELISA) both for IL-17-stimulated MKN28 cells treated with specific MAP kinase inhibitors and gastric biopsy cultures treated with a neutralizing IL-17 antibody. Serum from H. pylori -infected patients was tested for immunoglobulin G response to CagA by ELISA. Treatment of MKN28 cells with IL-17 caused activation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) but not other MAP kinases and had the downstream effects of AP-1 and NF-κB activation and IL-8 synthesis. Blocking ERK 1/2 activity inhibited AP-1-mediated, but not NF-κB-mediated, IL-8 induction. Enhanced activation of ERK 1/2 was seen in gastric epithelial cells isolated from H. pylori -infected patients in comparison to uninfected controls, and this was associated with high IL-8. These effects were even more pronounced in patients seropositive for CagA than in seronegative ones. In gastric biopsy cultures, the addition of a neutralizing IL-17 antibody decreased ERK 1/2 activation, thus resulting in a significant inhibition of IL-8. In H. pylori -colonized gastric epithelial cells, IL-17-induced IL-8 synthesis is associated with and depends at least in part on the activation of ERK 1/2 MAP kinase.
تدمد: 1098-5522
0019-9567
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e092c82e2da38cf480c6097da5c0f0f9Test
https://doi.org/10.1128/iai.00071-14Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....e092c82e2da38cf480c6097da5c0f0f9
قاعدة البيانات: OpenAIRE