HopQ impacts the integrin α5β1-independent NF-κB activation by Helicobacter pylori in CEACAM expressing cells

International Journal of Medical Microbiology : IJMM
Michael Hartmut FeigeM Naumann

Abstract

Helicobacter pylori infection persists in more than half of the world's population and represents a risk factor for peptic ulcer disease and gastric cancer. Virulent strains of H. pylori carry a cag pathogenicity island (cagPAI), which encodes a type IV secretion system (T4SS) with the capability to inject the effector protein cytotoxin-associated gene A (CagA) into eukaryotic cells. Colonisation of the gastric epithelium by H. pylori provokes direct activation of the proinflammatory and survival factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). We investigated the impact of host cell receptor integrin α5β1 and the bacterial adhesin HopQ on the NF-κB activation. We found that H. pylori induced early T4SS-dependent, but CagA-independent canonical NF-κB signalling in polarized, apical infected NCI-N87 cells. Integrin-dependent CagA translocation was hardly detectable, as integrin β1 was sparsely located at the apical surface of polarized NCI-N87 cells. Knockdown experiments indicated that integrin α5β1 and integrin linked kinase (ILK) were dispensable for NF-κB activation in H. pylori infection. Thus, there exists no common mechanism, which mediates integrin α5β1-dependent H. pylori-triggered CagA tra...Continue Reading

Citations

Mar 25, 2019·Oncoimmunology·Chamutal GurGilad Bachrach
Feb 20, 2019·Gastric Cancer : Official Journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association·Shuye LinYouyong Lu
Jul 6, 2021·Frontiers in Oncology·Kaisa CuiZhaohui Huang

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