Early MyD88-dependent induction of interleukin-17A expression during Salmonella colitis

A. Marijke Keestra, Ivan Godinez, Mariana N. Xavier, Maria G. Winter, Sebastian E. Winter, Renée M. Tsolis, Andreas J. Bäumler

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

The development of T helper 17 (TH17) 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 δγT cells, TH17 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.

Original languageEnglish (US)
Pages (from-to)3131-3140
Number of pages10
JournalInfection and Immunity
Volume79
Issue number8
DOIs
StatePublished - Aug 2011

Fingerprint

Interleukin-17
Colitis
Salmonella
Interleukin-23
T-Lymphocytes
Th17 Cells
Neutrophil Infiltration
Interleukin-1
Mucous Membrane
Infection
Myeloid Differentiation Factor 88
CXC Chemokines
Salmonella enterica
Interleukin-1 Receptors
Intestinal Mucosa
S Phase
Bacterial Infections
Pathology
Cytokines
Inflammation

ASJC Scopus subject areas

  • Immunology
  • Microbiology
  • Parasitology
  • Infectious Diseases

Cite this

Keestra, A. M., Godinez, I., Xavier, M. N., Winter, M. G., Winter, S. E., Tsolis, R. M., & Bäumler, A. J. (2011). Early MyD88-dependent induction of interleukin-17A expression during Salmonella colitis. Infection and Immunity, 79(8), 3131-3140. https://doi.org/10.1128/IAI.00018-11

Early MyD88-dependent induction of interleukin-17A expression during Salmonella colitis. / Keestra, A. Marijke; Godinez, Ivan; Xavier, Mariana N.; Winter, Maria G.; Winter, Sebastian E.; Tsolis, Renée M.; Bäumler, Andreas J.

In: Infection and Immunity, Vol. 79, No. 8, 08.2011, p. 3131-3140.

Research output: Contribution to journalArticle

Keestra, AM, Godinez, I, Xavier, MN, Winter, MG, Winter, SE, Tsolis, RM & Bäumler, AJ 2011, 'Early MyD88-dependent induction of interleukin-17A expression during Salmonella colitis', Infection and Immunity, vol. 79, no. 8, pp. 3131-3140. https://doi.org/10.1128/IAI.00018-11
Keestra, A. Marijke ; Godinez, Ivan ; Xavier, Mariana N. ; Winter, Maria G. ; Winter, Sebastian E. ; Tsolis, Renée M. ; Bäumler, Andreas J. / Early MyD88-dependent induction of interleukin-17A expression during Salmonella colitis. In: Infection and Immunity. 2011 ; Vol. 79, No. 8. pp. 3131-3140.
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