[Promotion of phagocytosis and prevention of phagosome-lysosome (P-L) fusion in human peripheral blood monocytes by serotype specific glycopeptidolipid (GPL) antigen of Mycobacterium avium complex (MAC)].

Mycobacterium avium complex (MAC) is one of the most important opportunistic pathogens co-infected with HIV (AIDS) and a typical intracellular parasitic bacteria similar to M. tuberculosis. It is also noticed that M. avium infection causes immunosuppression especially in the cellular immunity of host animals, and specific serotype-subspecies such as sero-2, -4 or -8 can be isolated frequently in human infection. Furthermore, the prognosis after infection differs by the serotypes and serotype-4 shows heavy infection in general, while serotype-16 shows rapid improvement. Therefore, we have been interested in the immunomodifying activity of surface glycopeptidolipid (GPL) antigen. However, to date, no information has been available on the virulence factor of MAC related directly with intracellular bactericidal activity. Recently, we have tested the effect of various GPLs purified form MAC complex on phagocytic processes of human peripheral blood monocytes (PBMC). We have used GPL-coated heat-killed staphylococcal cells to be phagocytosed by PBMC, and phagosome-lysosome (P-L) fusion was estimated by the acridine orange staining of fused vesicles including bacteria. It was revealed that the serotype-4, -12 and -17 GPLs showed strong phagocytosis promotion and marked inhibition of P-L fusion, while serotype-9, -13, -16 and -19 GPLs showed neither promotion of phagocytosis, nor inhibition of P-L fusion in phagocytic cells. Serotype-5, -7, -8 and -10 GPLs showed stimulation of both phagocytosis and P-L fusion, concomitantly. These effects may be due to unknown interaction between specific carbohydrate chain of MAC and phagocytic cell membranes, and serotype-4, -12 and -17 GPLs may be one of the possible virulence factors in MAC.