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Infection and Immunity, January 2009, p. 387-398, Vol. 77, No. 1
0019-9567/09/$08.00+0     doi:10.1128/IAI.00933-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Interleukin-23 Orchestrates Mucosal Responses to Salmonella enterica Serotype Typhimurium in the Intestine

Ivan Godinez,¹ Manuela Raffatellu,¹ Hiutung Chu,¹ Tatiane A. Paixão,^1,2 Takeshi Haneda,¹ Renato L. Santos,² Charles L. Bevins,¹ Renée M. Tsolis,¹ and Andreas J. Bäumler^1*

Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, California,¹ Departamento de Clínica e Cirurgia Veterinárias, Escola de Veterinária, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil²

Received 26 July 2008/ Returned for modification 3 September 2008/ Accepted 9 October 2008

Salmonella enterica serotype Typhimurium causes an acute inflammatory reaction in the ceca of streptomycin-pretreated mice that involves T-cell-dependent induction of gamma interferon (IFN-), interleukin-22 (IL-22), and IL-17 expression (genes Ifn-, Il-22, and Il-17, respectively). We investigated here the role of IL-23 in initiating these inflammatory responses using the streptomycin-pretreated mouse model. Compared to wild-type mice, the expression of IL-17 was abrogated, IL-22 expression was markedly reduced, but IFN- expression was normal in the ceca of IL-23p19-deficient mice during serotype Typhimurium infection. IL-23p19-deficient mice also exhibited a markedly reduced expression of regenerating islet-derived 3 gamma, keratinocyte-derived cytokine, and reduced neutrophil recruitment into the cecal mucosa during infection. Analysis of CD3⁺ lymphocytes in the intestinal mucosa by flow cytometry revealed that β T cells were the predominant cell type expressing the IL-23 receptor in naive mice. However, a marked increase in the number of IL-23 receptor-expressing T cells was observed in the lamina propria during serotype Typhimurium infection. Compared to wild-type mice, T-cell-receptor-deficient mice exhibited blunted expression of IL-17 during serotype Typhimurium infection, while IFN- expression was normal. These data suggested that T cells are a significant source, but not the sole source, of IL-17 in the acutely inflamed cecal mucosa of mice. Collectively, our results point to IL-23 as an important player in initiating a T-cell-dependent amplification of inflammatory responses in the intestinal mucosa during serotype Typhimurium infection.

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* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, CA 95616-8645. Phone: (530) 754-7225. Fax: (530) 754-7240. E-mail: ajbaumler{at}ucdavis.edu

Published ahead of print on 27 October 2008.

Editor: J. B. Bliska

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Infection and Immunity, January 2009, p. 387-398, Vol. 77, No. 1
0019-9567/09/$08.00+0     doi:10.1128/IAI.00933-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

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