Hydrogen peroxide release by OKIa1 (anti DR--monoclonal antibody) resistant alveolar macrophages in tuberculosis

Phorbol myristate acetate (PMA) triggered hydrogen peroxide (H2O2) release from alveolar macrophages and corresponding blood monocytes were studied as a whole, in active tuberculosis, inactive tuberculosis (treated), non-tuberculous lung disease patients and normal individuals. Irrespective of the study subjects, the alveolar macrophages produced less H2O2 than the corresponding blood monocytes. The alveolar macrophages that were resistant to OKIa1 (Anti-DR monoclonal antibody and complement treatment) produced an increased level of H2O2 than the control ascites and complement treated alveolar macrophages. Moreover, such increase in H2O2 release was not seen with peripheral blood monocytes; more than 90% monocytes were OKIa1 resistant population. These OKIa1 resistant alveolar macrophages are probably important in their metabolic, microbicidal and the immunological functions.