Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.0306194 on August 17, 2006

Published online before print August 17, 2006
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(Journal of Leukocyte Biology. 2007;81:403-411.)
© 2007 by Society for Leukocyte Biology

Exposure to LPS suppresses CD4+ T cell cytokine production in Salmonella-infected mice and exacerbates murine typhoid

Aparna Srinivasan and Stephen J. McSorley1

Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, and Center for Infectious Diseases and Translational Microbiology Research, University of Minnesota Medical School, McGuire Translational Research Facility, Minneapolis, Minnesota, USA

1 Correspondence: Dept. of Medicine, Div. of Gastroenterology, Hepatology and Nutrition, and Center for Infectious Diseases and Translational Microbiology Research, University of Minnesota Medical School, McGuire Translational Research Facility, Room 3-4006, 2001 6th St., SE, Minneapolis, MN 55455, USA. E-mail: mcsor002{at}umn.edu

ABSTRACT

A number of studies have documented suppression of lymphocyte activation in mice infected with Salmonella. Here, we describe incomplete activation of CD4+ T cells following intravenous injection of specific peptide and LPS into Salmonella-infected mice. Although antigen-specific CD4+ T cells were activated by peptide/LPS to increase surface CD69 expression, they did not produce IL-2 or TNF-{alpha}. Suppression of cytokine production did not require prolonged exposure of the T cells to the Salmonella-infected environment, was not antigen specific, but was dependent upon the presence of LPS during stimulation. These data suggest that Salmonella-infected mice are exquisitely sensitive to the generation of a suppressive environment following innate immune stimulation with LPS. In agreement with this interpretation, repeated low-dose administration of LPS caused uncontrolled replication of attenuated Salmonella in vivo.

Key Words: bacterial infection • IL-2 • tumor necrosis factor-{alpha}


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J. Leukoc. Biol. 2007 81: 401-402. [Full Text] [PDF]



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