Proregenerative Activity of IL-33 in Gastric Tissue Cells Undergoing Helicobacter Pylori -Induced Apoptosis

• Published in: International journal of molecular sciences 2020-03, Vol.21 (5), p.1801
• Main Authors: Gonciarz, Weronika, Krupa, Agnieszka, Chmiela, Magdalena
• Format: Article
• Language: English
• Subjects: Apoptosis; Bacteria; Bcl-x protein; Caspase-3; Cell adhesion & migration; Cell culture; Cell growth; Cell proliferation; Cytokines; Deoxyribonucleic acid; DNA; Enzyme-linked immunosorbent assay; Epithelial cells; Evaluation; Fibroblasts; gastric barrier; Glycine; Guinea pigs; Heat shock proteins; Helicobacter pylori; Homeostasis; il-33; Immune system; Infections; Inflammation; Inflammatory response; Kinases; Lymphoma; Mitochondrial DNA; Peptides; Physiology; Production methods; proliferation; siRNA; Tissue engineering; Wound healing
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21051801

Interleukin (IL)-33 is a proinflammatory mediator that alerts the host immune system to disorders in tissue homeostasis. Aim. To understand the role of IL-33 in modulating gastric tissue cell growth affected by ). Methods. IL-33 production in guinea pigs ) experimentally infected with was evaluated by ELISA or immunohistochemical staining. The proregenerative activity of IL-33 was evaluated using gastric epithelial cells and fibroblasts that were naive or transfected with IL-33 siRNA exposed to glycine acid extract antigenic complex (GE), as well as by measuring cell migration, proliferation, metabolic activity and apoptosis. Animals infected by responded with increased production of IL-33. Also, cells treated in vitro with GE released more IL-33 than cells that were unstimulated. Silencing IL-33 in cells resulted in downregulation of metabolic activity, adhesion, migration and proliferation, especially after treatment with GE, as well as upregulation of cells apoptosis associated with caspase 3 increase and Bcl-xL decrease, suggesting proregenerative activity of IL-33. Interestingly, upregulation of cell proliferation by IL-33 was Erk independent. Our results indicate that IL-33 may protect gastric tissue from loss of homeostasis caused by deleterious effects of components and the inflammatory response developed during infection.