Helicobacter pylori-Induced TLR9 Activation and Injury Are Associated With the Virulence-Associated Adhesin HopQ
Year: 2020
Type: article
Abstract: Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma. The H. pylori cancer-associated cag pathogenicity island (cag-PAI) encodes a type IV secretion system (T4SS), which translocates microbial DNA and activates TLR9; however, most cag-PAI+-infected persons do not develop cancer and cag-PAI-independent regulators of pathogenesis, including strain-specific adhesins, remain understudied. We defined the relationships between H. pylori HopQ adhesin allelic type, gastric injury, and TLR9 activation. Type I hopQ alleles were significantly associated with magnitude of injury, cag-T4SS function, and TLR9 activation. Genetic deletion of hopQ significantly decreased H. pylori-induced TLR9 activation, implicating this adhesin in H. pylori-mediated disease.
Language: English
Subfield: Surgery
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: Helicobacter Pylori and Gastrointestinal Biology, G2507688059, Molecular and Cellular Basis for Digestive Diseases, Type IV Protein Secretion in Helicobacter pylori, Chemical Biology of Infectious Diseases (CBID) Training Program, H. Pylori Relationship to Digestive Diseases and Cancer, H. pylori-induced Inflammation and Gastric Cancer
OpenAlex ID: W3108947694