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Mycobacterium avium infection of macrophages results in progressive suppression of interleukin-12 production in vitro and in vivo.
|Title||Mycobacterium avium infection of macrophages results in progressive suppression of interleukin-12 production in vitro and in vivo.|
|Publication Type||Journal Article|
|Year of Publication||2002|
|Authors||Wagner D, Sangari FJ, Kim S, Petrofsky M, Bermudez LE|
|Journal||Journal of leukocyte biology|
|Date Published||2002 Jan|
|Keywords||Animals, Cells, Cultured, Humans, Interleukin-10, Interleukin-12, Macrophages, Mice, Mycobacterium avium, Transforming Growth Factor beta, Tuberculosis|
Interleukin-12 (IL-12) has been shown to have an important role in the host defense against Mycobacterium avium. We sought to determine if human monocyte-derived macrophages produce IL-12 upon M. avium infection. Although IL-12 can be measured in supernatants of M. avium-infected macrophages at 24, 48, and 72 h following infection, intracellular staining showed that 24 to 48 h after infection, IL-12 was synthesized chiefly by uninfected macrophages in the monolayer, suggesting that M. avium infection inhibits IL-12 production. In addition, the data also suggest that the longer macrophage monolayers were infected, the less IL-12 they were able to produce. Stimulation of macrophages with IFN-gamma prior to infection with M. avium resulted in greater production of IL-12 compared with unstimulated macrophages. Culture supernatant of M. avium-infected macrophage monolayers, but not control macrophages, partially inhibited IL-12 production by IFN-gamma-stimulated macrophages. This partial inhibition was not reversed by anti-interleukin-10 (anti-IL-10) and anti-transforming growth factor beta 1 (anti-TGF beta 1)-neutralizing antibodies. M. avium infection of macrophages in vitro also suppressed IL-12 synthesis induced by Listeria monocytogenes infection. Immunohistochemistry staining of spleen of infected mice showed that IL-12 production by splenic macrophages was more pronounced in the beginning of the infection but decreased later. Our data indicate that M. avium infection of macrophages suppresses IL-12 production by infected cells and that the suppression was not a result of the presence of IL-10 and TGF beta 1 in the culture supernatant.
|Alternate Journal||J. Leukoc. Biol.|