Document 0125
 DOCN  M95B0125
 TI    Cytokine modulation alters pulmonary clearance of Rhodococcus equi and
       development of granulomatous pneumonia.
 DT    9511
 AU    Kanaly ST; Hines SA; Palmer GH; Department of Veterinary Microbiology
       and Pathology, Washington; State University, Pullman 99164-7040, USA.
 SO    Infect Immun. 1995 Aug;63(8):3037-41. Unique Identifier : AIDSLINE
       MED/95347819
 AB    Rhodococcus equi, a facultative intracellular bacterium, causes chronic,
       often fatal granulomatous pneumonia in young horses and in humans with
       AIDS. The inability of host alveolar macrophages to kill intracellular
       R. equi results in the development of granulomas and progressive loss of
       pulmonary parenchyma. Clearance of the organism from the lung requires
       functional CD4+ T cells. The purpose of this study was to identify the
       cytokine effector mechanisms that mediate clearance of R. equi from the
       lung. Mice were treated with monoclonal antibodies (MAbs) to either
       gamma interferon (IFN-gamma) or interleukin-4 (IL-4) to determine the
       role of endogenous production of these cytokines in pulmonary clearance
       of R. equi. Mice treated with an anti-IL-4 or isotype control MAb
       cleared R. equi by 21 days postinfection and expressed increased levels
       of IFN-gamma mRNA, as detected by transcriptional analysis of bronchial
       lymph node CD4+ T cells. In contrast, mice treated with the
       anti-IFN-gamma MAb failed to express detectable IFN-gamma mRNA,
       expressed increased levels of IL-4 mRNA, failed to clear pulmonary
       infection, and developed pulmonary granulomas with large numbers of
       eosinophils. The enhancement of IL-4 mRNA expression and a predominance
       of eosinophils in pulmonary lesions of anti-IFN-gamma-treated mice
       suggest that a nonprotective Th2 response in involved in disease
       pathogenesis. The association of increased bronchial lymph node CD4+
       T-cell IFN-gamma mRNA expression with pulmonary clearance of R. equi
       suggests that a Th1 response is protective.
 DE    Actinomycetales Infections/*IMMUNOLOGY  Animal  Female  Gene Expression
       Interferon Type II/*PHYSIOLOGY  Interleukin-4/*PHYSIOLOGY
       Lung/*IMMUNOLOGY/PATHOLOGY  Mice  Mice, Inbred BALB C
       Pneumonia/IMMUNOLOGY/*MICROBIOLOGY  Rhodococcus equi/*IMMUNOLOGY  RNA,
       Messenger/GENETICS  Support, Non-U.S. Gov't  Support, U.S. Gov't,
       Non-P.H.S.  Support, U.S. Gov't, P.H.S.  Th1 Cells/IMMUNOLOGY  Th2
       Cells/IMMUNOLOGY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).