C L An1, X P Su, A G Harmsen. 1. Department of Pathogen Biology, China Medical University, Shenyang 110001.
Abstract
OBJECTIVE: To define the cell populations contributing to inflammation-associated respiratory impairment in Pneumocystis carinii pneumonia (PCP). METHODS: The host inflammation response was observed in CD4+ T cell-depleted mice and in CD4+ and CD8+ T cell-depleted mice infected with P. carinii via intratracheal inoculation. RESULTS: Mice depleted of both CD4+ and CD8+ T cells developed infection with neither increased respiratory rate nor lung injury. In contrast, mice depleted of CD4+ T cells alone exhibited severe pulmonary inflammation, and increased respiratory rates. Respiratory compromise was associated with the presence of activated CD8+ cells and neutrophils in the BALF. CONCLUSION: The host's inflammatory cell response to P. carinii directly impairs pulmonary function and contributes to the pathogenesis of PCP, CD8+ T cells appear to play a major role.
OBJECTIVE: To define the cell populations contributing to inflammation-associated respiratory impairment in Pneumocystis carinii pneumonia (PCP). METHODS: The host inflammation response was observed in CD4+ T cell-depleted mice and in CD4+ and CD8+ T cell-depleted mice infected with P. carinii via intratracheal inoculation. RESULTS:Mice depleted of both CD4+ and CD8+ T cells developed infection with neither increased respiratory rate nor lung injury. In contrast, mice depleted of CD4+ T cells alone exhibited severe pulmonary inflammation, and increased respiratory rates. Respiratory compromise was associated with the presence of activated CD8+ cells and neutrophils in the BALF. CONCLUSION: The host's inflammatory cell response to P. carinii directly impairs pulmonary function and contributes to the pathogenesis of PCP, CD8+ T cells appear to play a major role.