Diacyltrehalose of Mycobacterium tuberculosis inhibits lipopolysaccharide- and mycobacteria-induced proinflammatory cytokine production in human monocytic cells

FEMS Microbiol Lett. 2007 Feb;267(1):121-8. doi: 10.1111/j.1574-6968.2006.00553.x. Epub 2006 Nov 29.

Abstract

The lipids located in the outer layer of Mycobacterium tuberculosis, which include sulfolipid, phthiocerol dimycocerosate (PDIM), diacyltrehalose, and polyacyltrehalose, may play a role in host-pathogen interactions. These lipids were purified using thin-layer chromatography, and their ability to induce proinflammatory cytokines in human monocytes and in a human acute monocytic leukemia cell line (THP-1) was examined. None of the lipids tested induced significant interleukin (IL)-12p40 or tumor necrosis factor (TNF)-alpha production in monocytic cells. Diacyltrehalose significantly inhibited lipopolysaccharide- and M. tuberculosis-induced IL-12p40, TNF-alpha, and IL-6 productions in human monocytes, whereas other lipids had no effect. However, diacyltrehalose was unable to inhibit peptidoglycan-induced IL-12p40 production. These results suggest that diacyltrehalose is a mycobacterial factor capable of modulating host immune responses.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Cells, Cultured
  • Chromatography, Thin Layer
  • Cytokines / biosynthesis*
  • Humans
  • Interleukin-12 Subunit p40 / biosynthesis
  • Interleukin-6 / biosynthesis
  • Lipids / immunology*
  • Lipids / isolation & purification
  • Monocytes / immunology*
  • Mycobacterium tuberculosis / chemistry
  • Mycobacterium tuberculosis / immunology*
  • Trehalose / analogs & derivatives*
  • Trehalose / immunology*
  • Trehalose / isolation & purification
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Cytokines
  • Interleukin-12 Subunit p40
  • Interleukin-6
  • Lipids
  • Tumor Necrosis Factor-alpha
  • Trehalose