ADP-heptose enables Helicobacter pylori to exploit macrophages as a survival niche by suppressing antigen-presenting HLA-II expression.
Sara ColettaGreta BattaggiaChiara Della BellaMatteo FurlaniMartina HaukeLarissa FaassMario M D'EliosChristine JosenhansMarina de BernardPublished in: FEBS letters (2021)
The persistence of Helicobacter pylori in the human gastric mucosa implies that the immune response fails to clear the infection. We found that H. pylori compromises the antigen presentation ability of macrophages, because of the decline of the presenting molecules HLA-II. Here, we reveal that the main bacterial factor responsible for this effect is ADP-heptose, an intermediate metabolite in the biosynthetic pathway of lipopolysaccharide (LPS) that elicits a pro-inflammatory response in gastric epithelial cells. In macrophages, it upregulates the expression of miR146b which, in turn, would downmodulate CIITA, the master regulator for HLA-II genes. Hence, H. pylori, utilizing ADP-heptose, exploits a specific arm of macrophage response to establish its survival niche in the face of the immune defense elicited in the gastric mucosa.
Keyphrases
- helicobacter pylori
- inflammatory response
- helicobacter pylori infection
- poor prognosis
- immune response
- toll like receptor
- case report
- lps induced
- lipopolysaccharide induced
- endothelial cells
- genome wide
- anti inflammatory
- binding protein
- adipose tissue
- induced pluripotent stem cells
- living cells
- single molecule
- quantum dots
- bioinformatics analysis