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Inhibition of Cytokine Release by Mycobacterium tuberculosis Phenolic Glycolipid Analogues
Author(s) -
Elsaidi Hassan R. H.,
Lowary Todd L.
Publication year - 2014
Publication title -
chembiochem
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.05
H-Index - 126
eISSN - 1439-7633
pISSN - 1439-4227
DOI - 10.1002/cbic.201402001
Subject(s) - glycan , glycolipid , glycoconjugate , mycobacterium tuberculosis , proinflammatory cytokine , chemistry , cytokine , nitric oxide , biochemistry , tuberculosis , microbiology and biotechnology , secretion , biology , immunology , glycoprotein , inflammation , medicine , organic chemistry , pathology
Infection by Mycobacterium tuberculosis causes tuberculosis, a disease characterized by alteration of host innate and adaptive immunity. These processes are mediated by a series of bacterial biomolecules, among which phenolic glycolipids (PGLs) and the related p ‐hydroxybenzoic acid derivatives have been suggested to play important roles. To probe the importance of structural features of these glycans on cytokine modulation, we synthesized three M. tuberculosis PGL analogues ( 1 – 3 ), which differ from the native glycoconjugates by possessing a simplified lipid algycone. The ability of 1 – 3 to modulate the release of proinflammatory cytokines (TNF‐α, IL‐1β, IL‐6, MCP‐1) and nitric oxide (NO) was evaluated. None of the compounds stimulated the secretion of these signalling molecules. However, all showed a Toll‐like Receptor 2‐mediated, concentration‐dependent inhibition profile that was related to the methylation pattern on the glycan.