TY - JOUR KW - Animals KW - Granuloma KW - Interferon-gamma KW - leprosy KW - Macrophages KW - Mice KW - Models, Immunological KW - Mycobacterium Infections KW - Mycobacterium avium KW - Mycobacterium bovis KW - Nitric Oxide KW - Nitric Oxide Synthase KW - Tuberculosis, Pulmonary AU - Cooper AM AU - Adams LW AU - Dalton D AU - Appelberg R AU - Ehlers S AB -

Granulomatous disease following exposure to Mycobacterium tuberculosis, Mycobacterium leprae or Mycobacterium avium is correlated with strong inflammatory and protective responses. The mouse model of mycobacterial infection provides an excellent tool with which to examine the inter-relationship between protective cell-mediated immunity and tissue-damaging hypersensitivity. It is well established that T cells and interferon (IFN)-gamma are necessary components of anti-bacterial protection. We propose that IFN-gamma also modulates the local cellular response by downregulating lymphocyte activation and by driving T cells into apoptosis, and that the events that limit excessive inflammation are largely mediated by IFN-gamma-induced nitric oxide (NO). In several murine models of mycobacterial infection, the absence of IFN-gamma and/or NO results in dysregulated granuloma formation and increased lymphocytic responses, which, in the case of M. avium infection, even leads to reduced bacterial growth.

BT - Trends in microbiology C1 - http://www.ncbi.nlm.nih.gov/pubmed/11973155?dopt=Abstract DA - 2002 May DO - 10.1016/s0966-842x(02)02344-2 IS - 5 J2 - Trends Microbiol. LA - eng N2 -

Granulomatous disease following exposure to Mycobacterium tuberculosis, Mycobacterium leprae or Mycobacterium avium is correlated with strong inflammatory and protective responses. The mouse model of mycobacterial infection provides an excellent tool with which to examine the inter-relationship between protective cell-mediated immunity and tissue-damaging hypersensitivity. It is well established that T cells and interferon (IFN)-gamma are necessary components of anti-bacterial protection. We propose that IFN-gamma also modulates the local cellular response by downregulating lymphocyte activation and by driving T cells into apoptosis, and that the events that limit excessive inflammation are largely mediated by IFN-gamma-induced nitric oxide (NO). In several murine models of mycobacterial infection, the absence of IFN-gamma and/or NO results in dysregulated granuloma formation and increased lymphocytic responses, which, in the case of M. avium infection, even leads to reduced bacterial growth.

PY - 2002 SP - 221 EP - 6 T2 - Trends in microbiology TI - IFN-gamma and NO in mycobacterial disease: new jobs for old hands. VL - 10 SN - 0966-842X ER -