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Salmonella SopB suppresses post-transcriptionally regulated cytokine release to reduce early tissue inflammation and delay disease progression

ABSTRACT: Salmonella enterica subsp. enterica serovar Typhimurium (S. Typhimurium) manipulates cellular processes through the translocation of effector molecules into the host cell cytosol. Using a recently established neonatal S. Typhimurium infection model, we provide functional insights into how Salmonella outer protein B (SopB) suppresses early mucosal tissue inflammation and prolongs host survival. Mechanistically, SopB prevents a disintegrin and metalloprotease 17 (ADAM17) activation, plasma membrane translocation and the release of membrane-bound TNFa from enterocytes and reduces epithelial secretion of IL-18 via mTOR-controlled secretory autophagy. This abolishes the early epithelial transcriptional response and reduces immune cell recruitment and programmed cell death-mediated mucosal barrier disruption delaying disease progression. The immunosuppressive effect of SopB is independent of the C-terminally encoded phosphatidylinositol phosphatase and phosphotransferase activity but requires an intact N-terminal domain. Thus, SopB suppresses the early, post-transcriptional regulation of epithelial cytokine release in an inositol phosphatase-independent manner likely promoting pathogen transmission.

ORGANISM(S): Mus musculus

PROVIDER: GSE326693 | GEO | 2026/04/06

REPOSITORIES: GEO

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Project description:InvF ChIP-chip on Salmonella enterica serovar Typhimurium SL1344 using anti-Myc antibody against strain with chromosomally 9Myc-tagged InvF (IP samples) and wildtype strain (mock IP samples) Salmonella enterica serovar Typhimurium causes a range of diseases from self-limiting gastroenteritis to life-threatening systemic infections. Its complex infection process is initiated by the invasion of the intestinal epithelial monolayer by means of a type three secretion system. InvF is one of the key regulators governing the invasion of epithelial cells. By mapping the InvF regulon, i.e. locating its direct target genes, the gene network underlying invasion can be further examined, including identifying possible new effector-encoding genes. In order to map the InvF regulon, we performed chromatin immunoprecipitation combined with tiling microarray analysis (ChIP-chip) and compared expression of the identified target genes in an invF mutant and a wildtype strain. In addition, the promoter regions of these target genes were searched for the presence of an InvF recognition site. Finally, a query-driven biclustering method, combined with a microarray compendium containing publically available S. Typhimurium gene expression data, was applied as an in silico validation technique for functional relatedness between newly identified target genes and known invasion genes. As expected, under invasion inducing conditions, InvF activates the expression of invasion chaperone encoding sicA and the effector-encoding genes sopB, sopE, sopE2 and sopA by binding their promoter region. Newly identified InvF targets are steB, encoding a secreted effector, and STM1239. The presence of an InvF recognition site in the promoter regions of these target genes further supports this observation. In addition, the query-driven biclustering method revealed similarities in expression profiles between STM1239 and known InvF regulated invasion genes over a range of experimental conditions. In conclusion, we here deliver the first evidence for direct binding of InvF to the promoter regions of sopA and sopE2, and associate genes encoding a secreted effector (steB) and a putative novel effector (STM1239) with the Salmonella invasion regulator InvF. Three IP samples (from three biological replicates using anti-Myc antibody against Salmonella Typhimurium SL1344 strain encoding chromosomally 9Myc-tagged InvF) and three control mock IP samples (from three biological replicates using anti-Myc antibody against Salmonella Typhimurium SL1344 wildtype strain) were labeled with Cy5 and hybridized against a common genomic DNA reference, labeled with Cy3, on 6 S. Typhimurium LT2 whole genome tiling arrays

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Salmonella SopB suppresses post-transcriptionally regulated cytokine release to reduce early tissue inflammation and delay disease progression

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