Open AccessDiacyltrehalose of Mycobacterium tuberculosis inhibits lipopolysaccharide‐ and mycobacteria‐induced proinflammatory cytokine production in human monocytic cells
Author(s) -
Lee KilSoo,
Dubey Vinod S.,
Kolattukudy Pappachan E.,
Song ChangHwa,
Shin ARum,
Jung SaetByel,
Yang ChulSu,
Kim SuYoung,
Jo EunKyeong,
Park JeongKyu,
Kim HwaJung
Publication year - 2007
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2006.00553.x
Subject(s) - proinflammatory cytokine , mycobacterium tuberculosis , lipopolysaccharide , microbiology and biotechnology , cytokine , tuberculosis , mycobacterium , immunology , biology , medicine , inflammation , pathology
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)‐α production in monocytic cells. Diacyltrehalose significantly inhibited lipopolysaccharide‐ and M. tuberculosis ‐induced IL‐12p40, TNF‐α, 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.