| Literature DB >> 33245103 |
Samuel D R Dooyema1,2, Uma S Krishna3, John T Loh3, Giovanni Suarez3, Timothy L Cover1,3,4, Richard M Peek1,3.
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.Entities:
Keywords: zzm321990 Helicobacter pylorizzm321990 ; HopQ; TLR9; gastric cancer; secretion systems
Mesh:
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Year: 2021 PMID: 33245103 PMCID: PMC8280490 DOI: 10.1093/infdis/jiaa730
Source DB: PubMed Journal: J Infect Dis ISSN: 0022-1899 Impact factor: 5.226