K Suzuki
I have studied pathogenesis of pulmonary Mycobacterium avium complex disease (PMAC), using mouse and human alveolar macrophage (PAM) model of the infection as well as clinical evaluations. The mouse model revealed no relation between natural resistance against the bacteria and the activation of macrophages which was evaluated on the basis of releasing capacities of prostaglandin E2 and superoxide anion. The PAM model suggested that TNF-alpha and GM-CSF could activate PAM to restrict the intracellular growth of the bacteria, probably not through the superoxide anion release, but through the myeloperoxidasae-halide system...
October 1997: Kekkaku: [Tuberculosis]