Clearance of Virulent but Not AvirulentRhodococcus equifrom the Lungs of Adult Horses Is Associated with Intracytoplasmic Gamma Interferon Production by CD4+and CD8+T Lymphocytes

American Society for Microbiology - Tập 10 Số 2 - Trang 208-215 - 2003
Stephen A. Hines1,2,3, Diana M. Stone1,2,3, Melissa T. Hines1,2,3, Debby C. Alperin1,2,3, Donald P. Knowles1,2,3, Linda K. Norton1,2,3, Mary Jo Hamilton1,2,3, William C. Davis1,2,3, Travis C. McGuire1,2,3
1Department of Veterinary Clinical Sciences, Washington State University
2Department of Veterinary Microbiology and Pathology
3USDA Agricultural Research Service Animal Disease Research Unit, Pullman, Washington 99164-7040

Tóm tắt

ABSTRACTRhodococcus equiis a gram-positive bacterium that infects alveolar macrophages and causes rhodococcal pneumonia in horses and humans. The virulence plasmid ofR. equiappears to be required for both pathogenicity in the horse and the induction of protective immunity. An understanding of the mechanisms by which virulentR. equicircumvents protective host responses and by which bacteria are ultimately cleared is important for development of an effective vaccine. Six adult horses were challenged with either virulentR. equior an avirulent, plasmid-cured derivative. By using a flow cytometric method for intracytoplasmic detection of gamma interferon (IFN-γ) in equine bronchoalveolar lavage fluid (BALF) cells, clearance of the virulent strain was shown to be associated with increased numbers of pulmonary CD4+and CD8+T lymphocytes producing IFN-γ. There was no change in IFN-γ-positive cells in peripheral blood, suggesting that a type 1 recall response at the site of challenge was protective. The plasmid-cured strain ofR. equiwas cleared in horses without a significant increase in IFN-γ-producing T lymphocytes in BALF. In contrast to these data, a previous report in foals suggested an immunomodulating role forR. equivirulence plasmid-encoded products in downregulating IFN-γ expression by equine CD4+T lymphocytes. Intracytoplasmic detection of IFN-γ provides a method to better determine whether modulation of macrophage-activating cytokines by virulent strains occurs uniquely in neonates and contributes to their susceptibility to rhodococcal pneumonia.

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