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Diacyltrehalose of Mycobacterium tuberculosis inhibits lipopolysaccharide- and mycobacteria-induced proinflammatory cytokine production in human monocytic cells
- Lee, Kil-Soo, Dubey, Vinod S., Kolattukudy, Pappachan E., Song, Chang-Hwa, Shin, A-Rum, Jung, Saet-Byel, Yang, Chul-Su, Kim, Su-Young, Jo, Eun-Kyeong, Park, Jeong-Kyu, Kim, Hwa-Jung
- FEMS microbiology letters 2007 v.267 no.1 pp. 121-128
- Mycobacterium tuberculosis, host-pathogen relationships, humans, immune response, interleukin-6, leukemia, lipids, monocytes, thin layer chromatography, tumor necrosis factor-alpha
- 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.