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

    Authors

    K. S. Lee; V. S. Dubey; P. E. Kolattukudy; C. H. Song; A. R. Shin; S. B. Jung; C. S. Yang; S. Y. Kim; E. K. Jo; J. K. Park;H. J. Kim

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    Abbreviated Journal Title

    FEMS Microbiol. Lett.

    Keywords

    Mycobacterium tuberculosis; diacyltrehalose; cytokines; monocytes; TOLL-LIKE RECEPTORS; PULMONARY TUBERCULOSIS; T-CELLS; ANTIGEN; LIPOARABINOMANNANS; INTERLEUKIN-12; MACROPHAGES; ACTIVATION; IMMUNITY; IL-12; Microbiology

    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.

    Journal Title

    Fems Microbiology Letters

    Volume

    267

    Issue/Number

    1

    Publication Date

    1-1-2007

    Document Type

    Article

    Language

    English

    First Page

    121

    Last Page

    128

    WOS Identifier

    WOS:000243235400018

    ISSN

    0378-1097

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