01976nas a2200253   4500000000100000008004100001653001300042653001500055653003300070653001000103653001700113100001000130700001700140700001400157700001400171700001200185700001100197700001500208245016200223300001200385490000800397520130300405022001401708       2016                            d10aCytokine10aMAP kinase10aMycobacterium indicus pranii10aTLR-410aTuberculosis1 aDas S1 aChowdhury BP1 aGoswami A1 aParveen S1 aJawed J1 aPal NK1 aMajumdar S00aMycobacterium indicus pranii (MIP) mediated host protective intracellular mechanisms against tuberculosis infection: Involvement of TLR-4 mediated signaling.  a201-2090 v1013 a<p>Mycobacterium tuberculosis infection inflicts the disease Tuberculosis (TB), which is fatal if left untreated. During M.&nbsp;tuberculosis infection, the pathogen modulates TLR-4 receptor down-stream signaling, indicating the possible involvement of TLR-4 in the regulation of the host immune response. Mycobacterium indicus pranii (MIP) possesses immuno-modulatory properties which induces the pro-inflammatory responses via induction of TLR-4-mediated signaling. Here, we observed the immunomodulatory properties of MIP against tuberculosis infection. We have studied the detailed signaling mechanisms employed by MIP in order to restore the host immune response against the in&nbsp;vitro tuberculosis infection. We observed that in infected macrophages MIP treatment significantly increased the TLR-4 expression as well as activation of its downstream signaling, facilitating the activation of P38 MAP kinase. MIP treatment was able to activate NF-κB via involvement of TLR-4 signaling leading to the enhanced pro-inflammatory cytokine and NO generation in the infected macrophages and generation of protective immune response. Therefore, we may suggest that, TLR4 may represent a novel therapeutic target for the activation of the innate immune response during Tuberculosis infection.</p>
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