Article abstract


Nature Medicine 14, 421 - 428 (2008)
Published online: 23 March 2008 | doi:10.1038/nm1743

Simian immunodeficiency virus–induced mucosal interleukin-17 deficiency promotes Salmonella dissemination from the gut

Manuela Raffatellu1,4, Renato L Santos1,4, David E Verhoeven1, Michael D George1, R Paul Wilson1, Sebastian E Winter1, Ivan Godinez1, Sumathi Sankaran1, Tatiane A Paixao1, Melita A Gordon2, Jay K Kolls3, Satya Dandekar1 & Andreas J Bäumler1


Salmonella typhimurium causes a localized enteric infection in immunocompetent individuals, whereas HIV-infected individuals develop a life-threatening bacteremia. Here we show that simian immunodeficiency virus (SIV) infection results in depletion of T helper type 17 (TH17) cells in the ileal mucosa of rhesus macaques, thereby impairing mucosal barrier functions to S. typhimurium dissemination. In SIV-negative macaques, the gene expression profile induced by S. typhimurium in ligated ileal loops was dominated by TH17 responses, including the expression of interleukin-17 (IL-17) and IL-22. TH17 cells were markedly depleted in SIV-infected rhesus macaques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemination. IL-17 receptor–deficient mice showed increased systemic dissemination of S. typhimurium from the gut, suggesting that IL-17 deficiency causes defects in mucosal barrier function. We conclude that SIV infection impairs the IL-17 axis, an arm of the mucosal immune response preventing systemic microbial dissemination from the gastrointestinal tract.

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  1. Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Avenue, Davis, California 95616-8645, USA.
  2. Division of Gastroenterology, Faculty of Medicine, University of Liverpool, First Floor Nuffield Building, Ashton Street, Liverpool L69 3BX, UK.
  3. Children's Hospital of Pittsburgh, Suite 3765, 3705 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
  4. These authors contributed equally to this work.

Correspondence to: Andreas J Bäumler1 e-mail: ajbaumler@ucdavis.edu




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