Increased lung cell cytotoxic but not bactericidal or phagocytic activity in Mycobacterium avium complex-infected mice.
Following intranasal infection of mice with Mycobacterium avium complex (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, H202, and 02- by 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 either in vitro or in vivo experiments. This study suggests that following intranasal infection with MAC, inflammatory cells are activated, sufficient to prevent further bacterial growth in vivo but not sufficient to clear the infection. We suggest that the deficiency may lie in the phagocytic activity of the cells.
Saunders
B M
BM
Microbiology Department, University of Melbourne, Parkville, Victoria, Australia.
Cheers
C
C
D000281:Administration, Intranasal; D000818:Animals; D003602:Cytotoxicity, Immunologic; D008087:Listeria / Q000276:immunology; D008168:Lung / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009162:Mycobacterium avium / Q000276:immunology* / Q000502:physiology*; D010586:Phagocytes / Q000276:immunology; D010587:Phagocytosis / Q000187:drug effects*; D014397:Tuberculosis, Pulmonary / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology