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Published on: January 5, 2016
Lipopolysaccharide is a potent monocyte/macrophage-specific stimulator of human immunodeficiency virus type 1
R J Pomerantz1, M B Feinberg, D Trono
1Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142.
Insights
Lipopolysaccharide (LPS) activates nuclear factor kappa B (NF-kappa B) in immune cells, significantly increasing HIV-1 production. This LPS-induced HIV-1 replication, particularly in monocyte/macrophage cells, highlights potential clinical relevance.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Lipopolysaccharide (LPS) is a potent immune stimulant.
- Human immunodeficiency virus type 1 (HIV-1) replication is complex and influenced by host factors.
- Monocyte/macrophage lineage cells play a critical role in HIV-1 pathogenesis.
Purpose of the Study:
- To investigate the effect of LPS on HIV-1 long terminal repeat (LTR) activity.
- To determine the role of nuclear factor kappa B (NF-kappa B) in LPS-mediated HIV-1 induction.
- To assess LPS's impact on HIV-1 production in different cell types.
Main Methods:
- Transfection of HIV-1-LTR CAT constructs into cell lines.
- Electrophoretic mobility shift assays (EMSA) to detect NF-kappa B activation.
- Measurement of HIV-1 production and RNA levels in chronically infected cell lines.
- Treatment with LPS and granulocyte/macrophage colony-stimulating factor (GM-CSF).
Main Results:
- LPS stimulated HIV-1-LTR constructs in monocyte/macrophage cell lines but not T cell lines.
- LPS induced NF-kappa B DNA binding activity in U937 and THP-1 cells.
- LPS dramatically increased HIV-1 production in GM-CSF-primed U1 cells, correlated with increased HIV-1 RNA and NF-kappa B activation.
- LPS did not induce HIV-1 production in a cloned T cell line.
Conclusions:
- LPS-induced NF-kappa B activation is a key mechanism for stimulating HIV-1 replication in monocyte/macrophage lineage cells.
- The synergistic effect of GM-CSF and LPS enhances HIV-1 production.
- LPS may play a clinically significant role in modulating HIV-1 disease progression at low concentrations.
Abstract:
Lipopolysaccharide (LPS) potently stimulates human immunodeficiency virus type 1-long terminal repeat (HIV-1-LTR) CAT constructs transfected into monocyte/macrophage-like cell lines but not a T cell line. This effect appears to be mediated through the induction of nuclear factor kappa B (NF-kappa B). Electrophoretic mobility shift assays demonstrate that LPS induces a DNA binding activity indistinguishable from NF-kappa B in U937 and THP-1 cells. LPS is also shown to dramatically increase HIV-1 production from a chronically infected monocyte/macrophage-like cloned cell line, U1, which produces very low levels of HIV-1 at baseline. The stimulation of viral production from this cell line occurs only if these cells are treated with granulocyte/macrophage colony-stimulating factor (GM-CSF) before treatment with LPS. This stimulation of HIV-1 production is correlated with an increase in the level of HIV-1 RNA and and activation of NF-kappa B. LPS is not able to induce HIV-1 production in a cloned T cell line. The effect of LPS on HIV-1 replication occurs at picogram per milliliter concentrations and may be clinically significant in understanding the variability of the natural history of HIV-1 infection.
