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* Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, and
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;
Department of Pathology, George Washington University, Washington, DC 20037, and
Department of Microbiology, Colorado State University, Fort Collins, CO 80523
In lymphoid tissues coinfected with Mycobacterium
avium complex (MAC) and HIV-1, increased viral replication has
been observed. This study investigates the role of MAC in perpetuating
both infections through the recruitment of monocytes as potential new
hosts for bacteria and HIV-1. Increased numbers of macrophages were
present in the lymph nodes of patients with dual infection as compared
with lymph nodes from HIV+ patients with no known
opportunistic pathogens. In a coculture system, monocyte-derived
macrophages were treated with HIV-1 or M. avium and its
constituents to further define the mechanism whereby MAC infection of
macrophages initiates monocyte migration. Monocyte-derived macrophages
treated with bacteria or bacterial products, but not HIV-1, induced a
rapid 2- to 3-fold increase in recruitment of monocytes. Pretreatment
of the monocytes with pertussis toxin inhibited the migration of these
cells, indicating a G protein-linked pathway is necessary for induction
of chemotaxis and thus suggesting the involvement of chemokines.
Analysis of chemokine mRNA and protein levels from M.
avium-treated cultures revealed MAC-induced increases in the
expression of IL-8, macrophage-inflammatory protein (MIP)-1
, and
MIP-1
with donor-dependent changes in monocyte chemotactic
protein-1. Pyrrolidine dithiocarbamate, an antioxidant, inhibited the
activation of NF-
B and significantly diminished the MAC-induced
chemotaxis, concurrently lowering the levels of monocyte chemotactic
protein-1 and MIP-1. These data demonstrate that MAC induces
macrophage production of multiple chemotactic factors via NF-B to
promote monocyte migration to sites of MAC infection. In vivo,
opportunistic infection may act as a recruitment mechanism in which
newly arrived monocytes serve as naive hosts for both MAC and HIV-1,
thus perpetuating both infections.
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