J Infect Dis. 2010 Jun 24. [Epub ahead of print]
Interleukin 17 Receptor Signaling Is Deleterious during Toxoplasma gondii Infection in Susceptible BL6 Mice
Guiton R, Vasseur V, Charron S, Arias MT, Van Langendonck N, Buzoni-Gatel D, Ryffel B, Dimier-Poisson I.
Unité Mixte de Recherche (UMR), 0483 Université, Institut National de la Recherche Agronomique (INRA), Immunologie Parasitaire et Vaccinologie, Biothérapies Anti-Infectieuses, Université François Rabelais, Unité de Formation et de Recherche des Sciences Pharmaceutiques, and 2Service de Parasitologie-Mycologie-Médecine Tropicale, Centre Hospitalier Régional et Universitaire, Tours, 3Unité de Recherche, 1282 Infectiologie Animale et Santé Publique, INRA-Centre de Tours, Nouzilly, and 4UMR 6218 Université-Centre National de la Recherche Scientifique, Immunologie et Embryologie Moléculaire, Orléans, France; and 5Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, South Africa.
Abstract
Th17 cells are involved in host defense against several pathogens. Using interleukin (IL) 17RA-deficient mice, we demonstrated reduced ileitis with diminished neutrophil recruitment and inflammatory lesions in the ileum, in the regional lymph node, in the spleen, and in the liver at day 7 and prolonged survival after Toxoplasma gondii infection. In addition, IL-17A antibody neutralization reduced inflammation and enhanced survival in BL6 mice. Diminished inflammation is associated with augmented interferon (IFN) gamma serum levels and enhanced production of IL-10 and IFN-gamma in cultured splenocytes upon antigen restimulation. Finally, cyst load and inflammation in the brain at 40 days are greater in surviving BL6 mice than in IL-17RA-deficient mice. In conclusion, oral T. gondii infection increases IL-17 expression and contributes to the inflammatory response, and IL-17 neutralization has a partial protective effect against fatal T. gondii-associated inflammation.
PMID: 20575661 [PubMed - as supplied by publisher]
No comments:
Post a Comment