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Helicobacter pylori-Induced Rev-erbα Fosters Gastric Bacteria Colonization by Impairing Host Innate and Adaptive Defense. | LitMetric

Helicobacter pylori-Induced Rev-erbα Fosters Gastric Bacteria Colonization by Impairing Host Innate and Adaptive Defense.

Cell Mol Gastroenterol Hepatol

National Engineering Research Center of Immunological Products, Department of Microbiology and Biochemical Pharmacy, College of Pharmacy and Laboratory Medicine, Third Military Medical University, Chongqing, China; Department of Gastroenterology, the Affiliated Hospital of Southwest Medical University, Luzhou, China. Electronic address:

Published: January 2022

AI Article Synopsis

  • - Rev-erbα is a transcriptional repressor that plays a significant role in immunity, but its effects on Helicobacter pylori infection are not well understood.
  • - In studies with infected patients and mice, Rev-erbα levels increased in gastric mucosa, and H. pylori infection activates its expression through specific signaling pathways, leading to higher bacterial colonization.
  • - The study concludes that Rev-erbα suppresses key antimicrobial proteins and chemokine responses, thereby reducing the ability of the immune system to clear H. pylori, which helps the bacteria persist in the gastric environment.

Article Abstract

Background & Aims: Rev-erbα represents a powerful transcriptional repressor involved in immunity. However, the regulation, function, and clinical relevance of Rev-erbα in Helicobacter pylori infection are presently unknown.

Methods: Rev-erbα was examined in gastric samples from H pylori-infected patients and mice. Gastric epithelial cells (GECs) were isolated and infected with H pylori for Rev-erbα regulation assays. Gastric tissues from Rev-erbα and wild-type (littermate control) mice or these mice adoptively transferred with CD4 T cells from IFN-γ and wild-type mice, bone marrow chimera mice and mice with in vivo pharmacological activation or inhibition of Rev-erbα were examined for bacteria colonization. GECs, CD45CD11cLy6GCD11bCD68 myeloid cells and CD4 T cells were isolated, stimulated and/or cultured for Rev-erbα function assays.

Results: Rev-erbα was increased in gastric mucosa of H pylori-infected patients and mice. H pylori induced GECs to express Rev-erbα via the phosphorylated cagA that activated ERK signaling pathway to mediate NF-κB directly binding to Rev-erbα promoter, which resulted in increased bacteria colonization within gastric mucosa. Mechanistically, Rev-erbα in GECs not only directly suppressed Reg3b and β-defensin-1 expression, which resulted in impaired bactericidal effects against H pylori of these antibacterial proteins in vitro and in vivo; but also directly inhibited chemokine CCL21 expression, which led to decreased gastric influx of CD45CD11cLy6GCD11bCD68 myeloid cells by CCL21-CCR7-dependent migration and, as a direct consequence, reduced bacterial clearing capacity of H pylori-specific Th1 cell response.

Conclusions: Overall, this study identifies a model involving Rev-erbα, which collectively ensures gastric bacterial persistence by suppressing host gene expression required for local innate and adaptive defense against H pylori.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8255816PMC
http://dx.doi.org/10.1016/j.jcmgh.2021.02.013DOI Listing

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