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Mediators of Inflammation
Volume 2017, Article ID 2432904, 12 pages
Research Article

MCL Plays an Anti-Inflammatory Role in Mycobacterium tuberculosis-Induced Immune Response by Inhibiting NF-κB and NLRP3 Inflammasome Activation

1Department of Immunology and Microbiology, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China
2Major in Biology, The University of British Columbia, Vancouver, Canada V6T 1Z4
3Department of Chemistry, School of Pharmacy, Fourth Military Medical University, Xi’an, Shaanxi 710034, China

Correspondence should be addressed to Yuejuan Zheng; moc.361@21467714631 and Xin Jiang; moc.361@oagnixgnaij

Received 6 December 2016; Accepted 28 March 2017; Published 31 May 2017

Academic Editor: Giuseppe Valacchi

Copyright © 2017 Qingwen Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mycobacterium tuberculosis (Mtb) remains a significant menace to global health as it induces granulomatous lung lesions and systemic inflammatory responses during active tuberculosis (TB). Micheliolide (MCL), a sesquiterpene lactone, was recently reported to have a function of relieving LPS-induced inflammatory response, but the regulative role of MCL on the immunopathology of TB still remains unknown. In this experiment, we examined the inhibitory effect of MCL on Mtb-induced inflammatory response in mouse macrophage-like cell line Raw264.7 by downregulating the activation of nuclear factor kappa B (NF-κB) and NLRP3 inflammasome. Evidences showed that MCL decreased the secretion of Mtb-induced inflammatory cytokines (IL-1β and TNF-α) in a dose-dependent manner. Meanwhile, MCL dramatically suppressed Mtb-induced activation of iNOS and COX2 as well as subsequent production of NO. Furthermore, MCL inhibited Mtb-induced phosphorylation of Akt (Ser 473) in Raw264.7. According to our results, MCL plays an important role in modulating Mtb-induced inflammatory response through PI3K/Akt/NF-κB pathway and subsequently downregulating the activation of NLRP3 inflammasome. Therefore, MCL may represent as a potential drug candidate in the adjuvant treatment of TB by regulating host immune response.