ArticleInfection and immunity2008
T cells help to amplify inflammatory responses induced by Salmonella enterica serotype Typhimurium in the intestinal mucosa.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 147 citations in OpenAlex.
- Review
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- Iron acquisition by a commensal bacterium modifies host nutritional immunity during Salmonella infection.Cell host & microbe · 2023Article
- Vaccine-induced inflammation and inflammatory monocytes promote CD4+ T cell-dependent immunity against murine salmonellosis.PLoS pathogens · 2023Article
- The microbiota conditions a gut milieu that selects for wild-type Salmonella Typhimurium virulence.PLoS biology · 2023Article
- Hacking the Immune Response to Solid Tumors: Harnessing the Anti-Cancer Capacities of Oncolytic Bacteria.Pharmaceutics · 2023Review
- Murine Models of Salmonella Infection.Current protocols · 2023Article
- Colonocyte-derived lactate promotes E. coli fitness in the context of inflammation-associated gut microbiota dysbiosis.Microbiome · 2022Article
- Host/microbiota interactions in health and diseases-Time for mucosal microbiology!Mucosal immunology · 2021Review
- Reshaping of bacterial molecular hydrogen metabolism contributes to the outgrowth of commensaleLife · 2021Article
- Induction of IL-22-Producing CD4+ T Cells by Segmented Filamentous Bacteria Independent of Classical Th17 Cells.Frontiers in immunology · 2021Article
- Sodium butyrate modulates chicken macrophage proteins essential for Salmonella Enteritidis invasion.PloS one · 2021Article
- Mechanism of the Gut Microbiota Colonization Resistance and Enteric Pathogen Infection.Frontiers in cellular and infection microbiology · 2021Review
32 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Salmonella enterica serotype Typhimurium causes an acute inflammatory reaction in the ceca of streptomycin-pretreated mice. We determined global changes in gene expression elicited by serotype Typhimurium in the cecal mucosa. The gene expression profile was dominated by T-cell-derived cytokines and genes whose expression is known to be induced by these cytokines. Markedly increased mRNA levels of genes encoding gamma interferon (IFN-gamma), interleukin-22 (IL-22), and IL-17 were detected by quantitative real-time PCR. Furthermore, the mRNA levels of genes whose expression is induced by IFN-gamma, IL-22, or IL-17, including genes encoding macrophage inflammatory protein 2 (MIP-2), inducible nitric oxide synthase (Nos2), lipocalin-2 (Lcn2), MIP-1alpha, MIP-1beta, and keratinocyte-derived cytokine (KC), were also markedly increased. To assess the importance of T cells in orchestrating this proinflammatory gene expression profile, we depleted T cells by using a monoclonal antibody prior to investigating cecal inflammation caused by serotype Typhimurium in streptomycin-pretreated mice. Depletion of CD3+ T cells resulted in a dramatic reduction in gross pathology, a significantly reduced recruitment of neutrophils, and a marked reduction in mRNA levels of Ifn-gamma, Il-22, Il-17, Nos2, Lcn2, and Kc. Our results suggest that T cells play an important role in amplifying inflammatory responses induced by serotype Typhimurium in the cecal mucosa.
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Registered trials
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