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. 2017 Jun 13;7:3431. doi: 10.1038/s41598-017-03477-3

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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OMS inhibits Mtb-induced inflammatory responses through AMPK activation. (a) BMDMs were infected with Mtb (moi = 10) for 4 h and then treated with OMS-A (1, 5, 10 μM) or OMS-B (1, 5, 10 μM) for 24 h. (b) BMDMs were transduced with adenoviral NF-ĸB-luciferase reporter plasmid for 36 h, and infected with Mtb and then treated with OMS-A or OMS-B for 6 h. The cells were harvested and NF-ĸB luciferase reporter activity was determined. (c) BMDMs were transduced with non-specific shRNA (shNS) or Ampk-specific shRNA (shAmpk)-expressing lentivirus for 48 h and then infected with Mtb, followed by treatment with OMS-A or OMS-B for 24 h. (a and c) The supernatants were harvested and subjected of ELISA analysis of TNF-α, IL-6, IL-1β, and IL-12p40 production. All data represent the means ± SD of triplicates from each sample. **p < 0.01, ***p < 0.001, compared with SC (a–c). U, uninfected/untreated; SC, solvent control; ns, no significant.