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RNA-seq data from mouse BMDMs infected with Salmonella enterica serovar Typhimurium

ABSTRACT: To investigate the gene expression profile of macrophages in response to Salmonella infection in vitro, we differentiated mouse BMDMs and the cells were used as a model for Salmonella infection We then performed gene expression profiling analysis using data obtained from RNA-seq of BMDMs at two conditions (uninfected and Salmonella-infected cells).

ORGANISM(S): Mus musculus

PROVIDER: GSE239543 | GEO | 2024/07/31

REPOSITORIES: GEO

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Project description:The gut microbiota is increasingly recognized for playing a critical role in human health and disease, especially in conferring resistance to both virulent pathogens such as Salmonella, which infects 1.2 million people in the United States every year [1], and opportunistic pathogens like Candida, which causes an estimated 46,000 cases of invasive candidiasis each year in the United States [2]. The dynamics of pathogen-microbiome interactions and the metabolites involved in this process remain largely unknown. We use gnotobiotic mice infected with the virulent pathogen Salmonella enterica serovar Typhimurium or the opportunistic pathogen Candida albicans in combination with metagenomics and discovery metabolomics to identify changes in the community and metabolome during infection. To isolate the role of the microbiota in response to pathogens, we compared mice monocolonized with the pathogen, uninfected mice 'humanized' with a synthetic human microbiome, or infected humanized mice. We observe that changes in the community and in biosynthetic gene cluster potential occur within 3 days for the virulent Salmonella enterica serovar Typhimurium, but there are minimal changes with a poorly colonizing Candida albicans. In addition, the metabolome shifts depending on infection status, including changes in glutathione metabolites in response to Salmonella infection. The LC-MS metabolomic fingerprint of the cecum differed between mice monocolonized with either pathogen and humanized infected mice. Specifically, we identified an increase in glutathione disulfide, glutathione cysteine disulfide, inosine 5'-monophosphate, and hydroxybutyrylcarnitine in mice infected with Salmonella in contrast to uninfected mice and mice monocolonized with Salmonella. These metabolites potentially play a role in pathogen-induced oxidative stress. These results provide insight into how the microbiota community members interact with each other and with pathogens on a metabolic level. Ref:[1] Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, and Griffin PM. Foodborne Illness Acquired in the United States—Major Pathogens. Emerg Infect Dis 2011;17:7-15. doi.org/10.3201/eid1701.P11101[2] Centers for Disease Control and Prevention, Antibiotic Resistance Threats in the United States, 2013

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.

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RNA-seq data from mouse BMDMs infected with Salmonella enterica serovar Typhimurium

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