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B in Different Cell Types Through Reactive Oxygen Intermediates
Cytokine Research Section Departments of
*
Molecular Oncology and
Bioimmunotherapy. University of Texas M. D. Anderson Cancer Center, Houston, TX 77030
Mycobacterium avium-intracellulare complex (MAC) is
one of the most common opportunistic pathogens in HIV-infected
patients. Their synergistic interaction leads to a rapid deterioration
of the host defense. In vivo, MAC manifests as a disseminated
granulomatous disease that produces a massive inflammatory tissue
response perhaps through its activation of inflammatory cytokines. The
intracellular signaling following interaction of the mycobacterium with
host cells is incompletely understood. Because the response is
dependent, in part, on the activation of NF-
B, we investigated the
effect of MAC on this nuclear transcription factor in cells of
macrophage and nonmacrophage lineage. We demonstrate that both high and
low virulence strains of MAC potently and rapidly activated NF-B. In
supershift assays, using specific Abs against the NF-B subunits, we
identified a p50/p65 heterodimer that was formed within 5 min after
incubation with the bacterium too rapidly for cytokines to be involved
in the activation. This activation was instead mediated through the
generation of reactive oxygen intermediates, inasmuch as preincubation
of cells with a variety of antioxidants inhibited NF-B activation.
Likewise, the transfection of cells with Mn-superoxide dismutase
blocked the NF-B activation induced by the bacterium. These data
suggest that NF-B activation is a consequence of interaction of host
cells with the bacterium and that the interaction may play a pivotal
role in the pathogenesis of the disease.
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