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*
Division of Pulmonary and Critical Care Medicine and Bellevue Chest Service,
Department of Pathology, New York University Medical Center, New York, NY 10016;
Department of Medicine, Sendai Kosei Hospital, Sendai, Japan;
§
Department of Microbiology and Infection, Institute of Medical Science, Tokyo University, Tokyo, Japan; and
¶
Public Health Research Institute, New York, NY 10016
HIV-1 replication is inhibited in uninflamed lung macrophages and
is stimulated during tuberculosis. Attempts to recapitulate activation
of HIV-1 replication in primary monocytes and macrophages ex vivo and
in the untreated and PMA-treated THP-1 cell line model in vitro have
produced opposite results depending on the state of differentiation of
the cells. After infection with Mycobacterium
tuberculosis, monocytes enhanced HIV-1 replication and produced
a stimulatory 37-kDa CCAAT/enhancer binding protein ß (C/EBPß)
transcription factor, whereas macrophages suppressed HIV-1 replication
and produced an inhibitory 16-kDa C/EBPß transcription factor.
IFN-ß induced inhibitory 16-kDa C/EBPß in macrophages, but had no
effect on C/EBPß expression in monocytes. Macrophages, but not
monocytes, were able to activate IFN-stimulated gene factor-3 (ISGF-3),
a transcription factor composed of STAT-1, STAT-2, and IFN regulatory
factor (IRF)-9, after infection with M. tuberculosis or
stimulation with type I IFN. Macrophages expressed IRF-9 DNA-binding
activity, but monocytes did not, and addition of the IRF-9 component
reconstituted ISGF-3 in extracts of IFN-treated monocytes. Modulation
of IFN responsiveness upon differentiation occurred at least in part
through a post-transcriptionally regulated increase in IRF-9
expression. Both monocytes and macrophages maintained IFN
responsiveness, activating STAT-1 homodimer formation and transcription
of the STAT-1 gene after IFN stimulation. In addition, both monocytes
and macrophages were able to activate NF-
B upon infection with
M. tuberculosis. These results show that induction of
ISGF-3, expression of the inhibitory 16-kDa C/EBPß, and suppression
of HIV-1 replication via a transcriptional mechanism are
macrophage-specific responses to infection with M.
tuberculosis.
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