• Svetlana O Carrigan, Yong Jun Yang, Thomas Issekutz, Nicholas Forward, David Hoskin, Brent Johnston, and Tong-Jun Lin.
• Department of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada.
• Immunobiology. 2009 Jan 1;214(3):211-22.

AbstractPseudomonas aeruginosa is a common cause of lung infection in immune compromised individuals. Studies in humans and mice have demonstrated that P. aeruginosa lung infection is associated with a predominant Th2 immune response, whereas Th1 responses are accompanied by a better pulmonary outcome. Regulatory T cells (Tregs) are a subpopulation of T cells with unique immunologic characteristics that suppress effector T cell functions. Whether Tregs contribute to P. aeruginosa-induced host responses has not been studied previously. We found that P. aeruginosa lung infection induced an increase in natural Treg cells (CD4+CD25+FOXP3+ T cells) in the spleen of mice. To investigate a role of natural CD4+CD25+ Tregs in the host response to P. aeruginosa lung infection in vivo, anti-CD25 Ab was used to deplete endogenous CD4+CD25+ Tregs. Anti-CD25 treatment depleted 90% of CD4+CD25+FOXP3+ cells. Surprisingly, no differences of P. aeruginosa-induced NF-kappaB activation and cytokine/chemokine production (IL-1beta, TNF, IL-6, IL-10, RANTES or MIP-2) were observed between anti-CD25-treated and isotype control Ab-treated animals. Similarly, no differences in lung histology and airway neutrophil infiltration were observed between anti-CD25 and control Ab-treated animals. Furthermore, no difference in survival outcome was found between anti-CD25 and control Ab-treated animals. These data demonstrate that although P. aeruginosa lung infection causes an increase of Tregs, the endogenous natural CD4+CD25+ Treg cells do not contribute significantly to the host response to this bacterium.

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