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A C-Terminal coiled-coil region of CagL is responsible for Helicobacter Pylori-induced Il-8 expression.
Eur. J. Micr. Imm. 6, 186-196 (2016)
Interleukin-8 (IL-8) is a potent neutrophil-activating chemokine which triggers the infiltration and migration of neutrophils into areas of bacterial infection. Helicobacter pylori-infected patient studies as well as animal models have revealed that H. pylori type I strains carrying an intact cytotoxin-associated gene pathogenicity island (cag-PAI) with a functional type IV secretion system (T4SS) induce IL-8 expression and secretion in gastric mucosa. This gastric mucosal IL-8 expression correlates with severe histological changes due to H. pylori infection. In the present study, we explored a new recognition pattern on the bacterial adhesion protein CagL inducing IL-8 expression in H. pylori-infected host cells. To analyze the secreted IL-8 concentration, we performed IL-8 enzyme-linked immunosorbent assay (ELISA). To investigate the H. pylori-induced IL-8 expression on the transcriptional level, we transiently transfected gastric epithelial cells (AGS) with a human IL-8 luciferase reporter construct. The results of this study demonstrate that specifically the C-terminal coiled-coil region of the H. pylori CagL protein, a protein described to be located on the tip of the T4SS-pilus, is responsible for several in vitro observations: 1) H. pylori-induced IL-8 secretion via the transforming growth factor (TGF)-α activated epidermal growth factor-receptor (EGF-R) signaling pathway; 2) H. pylori-induced elongation of the cells, a typical CagA-induced phenotype; and 3) the bridging of the T4SS to its human target cells. This novel bacterial-host recognition sequence allows a new insight into how H. pylori induces the inflammatory response in gastric epithelial cells and facilitates the development of precancerous conditions.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Cagl ; Helicobacter Pylori ; Il-8 ; Coiled-coil
ISSN (print) / ISBN
2062-509X
e-ISSN
2062-8633
Quellenangaben
Volume: 6,
Issue: 3,
Pages: 186-196
Publisher
Springer
Publishing Place
Budapest
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Pathology (PATH)