Laboratory of Bacterial Pathogenesis, Kuzell Institute for Arthritis and Infectious Diseases, California Pacific Medical Center Research Institute, San Francisco, California
Correspondence: Dr. Luiz E. Bermudez, Kuzell Institute, 2200 Webster Street, Suite 305, San Francisco, CA 94115. E-mail: luizb{at}cooper.cpmc.org
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-
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--stimulated macrophages. This partial inhibition
was not reversed by antiinterleukin-10 (anti-IL-10) and
antitransforming growth factor ß1 (anti-TGFß1)-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 TGFß1 in
the culture supernatant.
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