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Microb Pathog. 2011 Jun;50(6):350-9. doi: 10.1016/j.micpath.2011.03.001. Epub 2011 Mar 23.

Mycobacterium tuberculosis lipoarabinomannan enhances LPS-induced TNF-α production and inhibits NO secretion by engaging scavenger receptors.

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  • 1Nencki Institute of Experimental Biology, Laboratory of Plasma Membrane Receptors, 3 Pasteur St., 02-093 Warsaw, Poland.


Lipoarabinomannan capped with terminal oligomannosides (ManLAM) is a component of mycobacteria cell wall enabling Mycobacterium tuberculosis to infect macrophages. We found that short treatment (3.5h) of macrophage-like J774 cells and thioglycollate-elicited peritoneal murine macrophages with ManLAM and its deacylated form enhanced LPS-stimulated release of tumor necrosis factor-α (TNF-α). In contrast, prolong incubation of J774 cells with ManLAM (16h) led to inhibition of LPS-stimulated TNF-α production. LPS-triggered secretion of nitric oxide (NO) was suppressed by ManLAM and its deacylated form. Effects of ManLAM and its deacylated derivative were mimicked by dextran sulfate, a general ligand of scavenger receptors. The enhancement of LPS-induced TNF-α production by dextran sulfate was partially reversed by an antibody neutralizing scavenger receptor SR-PSOX/CXCL16 while the stimulatory activity of deacylated ManLAM was reversed by an antibody neutralizing class B scavenger receptor CD36. Our data suggest that CD36 mediates the activity of ManLAM and its deacylated form leading to TNF-α release in LPS-stimulated J774 cells and peritoneal murine macrophages, while NO production is modulated by unknown scavenger receptors.

Copyright © 2011 Elsevier Ltd. All rights reserved.

[PubMed - indexed for MEDLINE]
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