|Knowles Jr, Donald|
Submitted to: Clinical and Diagnostic Laboratory Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/24/2002
Publication Date: 10/24/2002
Citation: Clin. Diagn. Lab. Immunol. 10(02)2003 208-215
Interpretive Summary: Rhodococcus equi is a major cause of fulminating pnemonia in foals, often leading to death. A method was developed to detect IFN-gamma in the cytoplasma of cells and was used to study whether modulation of macrophage activating factors impact disease progression. It was found that IFN gamma in lung fluid cells was associated with clearance of a virulent strain of R. equi.
Technical Abstract: Rhodococcus equi is a gram-positive bacterium that infects alveolar macrophages and causes rhodococcal pneumonia in horses and humans. The virulence plasmid of R. equi appears to be required for both pathogenicity in the horse and the induction of protective immunity. An understanding of the mechanisms by which virulent R. equi circumvents 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 virulent R. equi or an avirulent, plasmid-cured derivative. By using a flow cytometric method for intracytoplasmic detection of gamma interferon (IFN-Y) in equine bronchoalveolar lavage fluid (HALF) cells, clearance of the virulent strain was shown to be associated with increased numbers of pulmonary CD4 + and CDS+ T lymphocytes producing IFN-Y. There was no change in IFN-Y-positive cells in peripheral blood, suggesting that a type 1 recall response at the site of challenge was protective. The plasmid-cured strain of R. equi was cleared in horses without a significant increase in IFN-Y-producing T lymphocytes in BALF. In contrast to these data, a previous report in foals suggested an immunomodulating role for R. equi virulence plasmid-encoded products in downregu- lating IFN-Y expression by equine CD4+ T lymphocytes. Intracytoplasmic detection of IFN-Y 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.