Activation of human monocyte--derived macrophages with lipopolysaccharide decreases human immunodeficiency virus replication in vitro at the level of gene expression.

Bernstein, Mariana; Tong-Starksen, Sandra; Locksley, Richard M.

doi:10.1172/jci115337

Cited by 86 publications

(70 citation statements)

References 42 publications

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“…Surprisingly, the opposite effect was observed when THP-1 cells were differentiated to macrophage-like cells by PMA treatment. Repression requires intact C/EBP sites and is associated with induction of an inhibitory 16-kDa C/EBP␤ (15,22). In the present study primary monocytes differentiated to macrophages by M-CSF also suppressed HIV-1 replication after infection with mycobacteria and were able to induce the inhibitory C/EBP␤.…”

Section: Discussionsupporting

confidence: 58%

“…Mutation of the C/EBP sites in the LTR produces a virus that continues to replicate in lymphocytes, but is no longer able to replicate in macrophages (21). Monocytic THP-1 cells and primary monocytes are able to up-regulate HIV-1 replication after infection with M. tuberculosis or stimulation with LPS (11,22). The enhancing effects of proinflammatory stimuli require intact C/EBP and NF-B sites in the HIV-1 LTR (6, 7).…”

Section: Discussionmentioning

confidence: 99%

“…The C/EBP sites in the LTR are required for LTR promoter function and viral replication in monocytes, but not lymphocytes (20,21). The negative regulatory element is the DNA element responsible for suppressing the HIV-1 LTR in macrophages after LPS stimulation (22). The negative regulatory element contains binding sites for the C/EBP transcription factor family (23).…”

Section: Differentiation Of Monocytes To Macrophages Switches the Mycmentioning

confidence: 99%

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Differentiation of Monocytes to Macrophages Switches theMycobacterium tuberculosisEffect on HIV-1 Replication from Stimulation to Inhibition: Modulation of Interferon Response and CCAAT/Enhancer Binding Protein β Expression

Weiden

Tanaka

Qiao³

et al. 2000

The Journal of Immunology

118

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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 β (C/EBPβ) transcription factor, whereas macrophages suppressed HIV-1 replication and produced an inhibitory 16-kDa C/EBPβ transcription factor. IFN-β induced inhibitory 16-kDa C/EBPβ in macrophages, but had no effect on C/EBPβ 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-κB upon infection with M. tuberculosis. These results show that induction of ISGF-3, expression of the inhibitory 16-kDa C/EBPβ, and suppression of HIV-1 replication via a transcriptional mechanism are macrophage-specific responses to infection with M. tuberculosis.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Section: Differentiation Of Monocytes To Macrophages Switches the Mycmentioning

confidence: 99%

See 1 more Smart Citation

Differentiation of Monocytes to Macrophages Switches theMycobacterium tuberculosisEffect on HIV-1 Replication from Stimulation to Inhibition: Modulation of Interferon Response and CCAAT/Enhancer Binding Protein β Expression

Weiden

Tanaka

Qiao³

et al. 2000

The Journal of Immunology

118

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“…Nucleoprotein complexes were resolved by gel retardation assays. Similar results were obtained in U937A cells and in PBMCs obtained as described (Bernstein et al, 1991). mutant (Table 1).…”

Section: The Ggtca Palindrome Forms Complexes With Nuclear Extracts Fsupporting

confidence: 86%

The GGTCA palindrome and cognate cellular factors in trans-regulation of human immunodeficiency virus long terminal repeat by herpes simplex virus

Feng

Kulka²,

Aurelian

1993

Journal of General Virology

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Molecular interactions between herpes simplex virus type 1 (HSV-1) and human immunodeficiency virus (HIV) were investigated in the promonocytic cell line U937. HSV-l-mediated activation was observed in transient expression assays with hybrid constructions containing the HIV long terminal repeat (LTR)-directed chloramphenicol aeetyltransferase gene. Comparison of constructions that differ in the GGTCA palindrome located within the negative regulatory region of the LTR revealed four-to eightfold lower activation levels for the wild-type as compared to the mutant sequence. Three protein species, 37K, 59K/64K and 75K, that bind to the wild-type GGTCA palindrome were resolved in nuclear extracts of uninfected U937 cells by gel retardation and u.v.-crosslinking experiments. The 37K protein did not bind to the mutant palindrome sequence. However, a distinct 120K protein was detected. The 37K and 59K/64K binding proteins were not resolved in similar experiments performed with nuclear extracts from HSV-l-infected U937 cells but there was a novel p50 species that binds only to the wild-type palindrome sequence. These findings raise the possibility that interaction of these proteins at the GGTCA palindrome is involved in HSV-l-mediated regulation of the HIV LTR in U937 cells.

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“…These cells are 99% viable and up to 94% peroxidase-positive by cytostaining [19]. Cultured MN (CM) were prepared as described before [20]. MN were cultured in complete IMDM containing 30% AIM V medium (Gibco BRL, Life Technologies, Grand Island, NY, USA) in polytetra¯uoroethylene (Te¯on, Savillex Corp., Minneapolis, MN, USA) jars at a concentration of 2´10 6 /2 ml for 14 days.…”

Section: Methodsmentioning

confidence: 99%

Modulation of Transforming Growth Factor β‐1 Gene Expression by Interleukin‐12

Wilkinson

Aung

et al. 2000

Scand J Immunol

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The interaction of cytokines and their net balance with regard to macrophage activation (or deactivation) and immune stimulation (or suppression), ultimately determines the success of host-immune response at sites of active infection. A regulatory role for interleukin (IL)-12 in production of transforming growth factor (TGF)-b1 has been suggested, however, remains controversial. In this study, we analyzed the effect of IL-12 on TGFb1 expression in the human lines, K562 and A549, and in primary human monocytes and macrophages. We found that IL-12 down-regulates TGF-b1 mRNA expression in K562, monocytes and bone marrow cells, and to a lesser extent in the A549 cells. Using constructs containing different regions of the ®rst promoter of the TGF-b1 gene and a reporter gene, we also demonstrate that this effect is mediated through the TGF-b1 gene promoter in the K562 and monocytic cell types. In conclusion, the critical role of IL-12 in the early activation of the immune response to pathogens may include down-modulation of TGF-b1 gene activity.

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Activation of human monocyte--derived macrophages with lipopolysaccharide decreases human immunodeficiency virus replication in vitro at the level of gene expression.

Cited by 86 publications

References 42 publications

Differentiation of Monocytes to Macrophages Switches theMycobacterium tuberculosisEffect on HIV-1 Replication from Stimulation to Inhibition: Modulation of Interferon Response and CCAAT/Enhancer Binding Protein β Expression

Differentiation of Monocytes to Macrophages Switches theMycobacterium tuberculosisEffect on HIV-1 Replication from Stimulation to Inhibition: Modulation of Interferon Response and CCAAT/Enhancer Binding Protein β Expression

The GGTCA palindrome and cognate cellular factors in trans-regulation of human immunodeficiency virus long terminal repeat by herpes simplex virus

Modulation of Transforming Growth Factor β‐1 Gene Expression by Interleukin‐12

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