Increased Lung Cell Cytotoxic but Not Bactericidal or Phagocytic Activity inMycobacterium aviumComplex-Infected Mice

Following intranasal infection of mice withMycobacterium aviumcomplex (MAC) organisms, bacterial growth plateaued at the fourth week postinfection and then remained relatively constant thereafter. Inflammatory cell numbers in the lungs increased 10-fold by 4 weeks postinfection, and lung cell cytotoxicity and the production of NO, H2O2, and O−2by lung cell cultures had all increased significantly by this time and remained elevated throughout the 15-week experimental study. Although these parameters are generally associated with increased bactericidal activity, there appeared to be a defect in phagocytosis by lung cells, so that bactericidal activity could not be demonstrated in eitherin vitroorin vivoexperiments. This study suggests that following intranasal infection with MAC, inflammatory cells are activated, sufficient to prevent further bacterial growthin vivobut not sufficient to clear the infection. We suggest that the deficiency may lie in the phagocytic activity of the cells.