ArticleInfection and immunity2011
Early MyD88-dependent induction of interleukin-17A expression during Salmonella colitis.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
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- Vaccine-induced inflammation and inflammatory monocytes promote CD4+ T cell-dependent immunity against murine salmonellosis.PLoS pathogens · 2023Article
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- An Experimental Approach to Rigorously Assess Paneth Cell α-Defensin (Defa) mRNA Expression in C57BL/6 Mice.Scientific reports · 2019Article
- T cell fate followingCommunications biology · 2019Article
- Novel Role of VisP and the Wzz System during O-Antigen Assembly in Salmonella enterica Serovar Typhimurium Pathogenesis.Infection and immunity · 2018Article
- The Immunoregulation of Th17 in Host against Intracellular Bacterial Infection.Mediators of inflammation · 2018Review
- Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion.Science (New York, N.Y.) · 2017Article
- Yin and yang of interleukin-17 in host immunity to infection.F1000Research · 2017Review
- Cytokines IL-17 and IL-22 in the host response to infection.Pathogens and disease · 2016Review
- Protective Immunity Elicited by Oral Immunization of Mice withFrontiers in cellular and infection microbiology · 2016Article
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- Now you see me, now you don't: the interaction of Salmonella with innate immune receptors.Nature reviews. Microbiology · 2015Review
- ELMO1 has an essential role in the internalization ofCellular and molecular gastroenterology and hepatology · 2015Article
- The mucosal inflammatory response to non-typhoidal Salmonella in the intestine is blunted by IL-10 during concurrent malaria parasite infection.Mucosal immunology · 2014Article
- Salmonella enterica Serovar Typhi conceals the invasion-associated type three secretion system from the innate immune system by gene regulation.PLoS pathogens · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The development of T helper 17 (T(H)17) cells is a well-established adaptive mechanism for the production of interleukin-17A (IL-17A), a cytokine involved in neutrophil recruitment. However, pathways contributing to mucosal expression of IL-17A during the initial phase of a bacterial infection have received less attention. Here we used the mouse colitis model of Salmonella enterica serotype Typhimurium infection to investigate the contribution of myeloid differentiation primary response protein 88 (MyD88) to inflammation and mucosal IL-17A expression. Expression of IL-23 in the cecal mucosa during S. Typhimurium colitis was dependent on the presence of MyD88. Furthermore, initial expression of IL-17A at 24 h after S. Typhimurium infection was dependent on MyD88 and the receptor for IL-1β. IL-23 and IL-1β synergized in inducing expression of IL-17A in splenic T cells in vitro. In the intestinal mucosa, IL-17A was produced by three distinct T cell populations, including δγ T cells, T(H)17 cells, and CD4(-)CD8(-) T cells. The absence of IL-1β signaling or IL-17 signaling reduced CXC chemokine expression but did not alter the overall severity of pathological lesions in the cecal mucosa. In contrast, cecal pathology and neutrophil recruitment were markedly reduced in Myd88-deficient mice during the initial phases of S. Typhimurium infection. Collectively, these data demonstrate that MyD88-dependent mechanisms, including an initial expression of IL-17A, are important for orchestrating early inflammatory responses during S. Typhimurium colitis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.