Helicobacter pylori-Induced TLR9 Activation and Injury Are Associated With the Virulence-Associated Adhesin HopQ. (27th November 2020)

• Record Type: Journal Article
• Authors: Dooyema, Samuel D R; Krishna, Uma S; Loh, John T; Suarez, Giovanni; Cover, Timothy L; Peek, Richard M
• Is Part Of: Journal of infectious diseases. Volume 224:Number 2(2021)
• Page Start: 360
• Page End: 365
• Publication Date: 2020-11-27
• Subjects: Helicobacter pylori -- gastric cancer -- HopQ -- TLR9 -- secretion systems; Communicable diseases -- Periodicals; Diseases -- Causes and theories of causation -- Periodicals; Medicine -- Periodicals; Communicable Diseases -- Periodicals; Electronic journals; 616.9
• DOI: 10.1093/infdis/jiaa730
• Languages: English
• ISSNs: 0022-1899

Abstract

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.