@article{29412,
  keywords = {Animals, Chemokine CXCL10, Female, Macrophage Activation, Macrophages, Peritoneal, Male, Mice, Mice, Inbred BALB C, Mycobacterium, Myeloid Differentiation Factor 88, NF-kappa B, Nod2 Signaling Adaptor Protein, Toll-Like Receptor 2},
  author = {Pandey RK and Sodhi A and Biswas SK and Dahiya Y and Dhillon M},
  title = {Mycobacterium indicus pranii mediates macrophage activation through TLR2 and NOD2 in a MyD88 dependent manner.},
  abstract = {<p>Mycobacterium indicus pranii (MIP) is a non-pathogenic strain of mycobacterium and has been used as a vaccine against tuberculosis and leprosy. Here, we investigated the role of different pattern recognition receptors in the recognition of heat-killed MIP by macrophages. Treatment of macrophages with MIP caused upregulation of pro-inflammatory cytokines (like TNFα and IL-1β) which was mediated through both TLR2 and NOD2, as revealed by our knockdown and/or knockout studies. Mechanistically, MIP-induced macrophage activation was shown to result in NF-κB activation and drastically abrogated by MyD88 deficiency, suggesting its regulation via an MyD88-dependent, NF-κB pathway. Interestingly, the IFN-inducible cytokine, CXCL10, which is known target of the TRIF-dependent TLR pathway was found to be upregulated in response to MIP but, in an MyD88-dependent manner. Collectively, these results demonstrate macrophages to recognize and respond to MIP through a TLR2, NOD2 and an MyD88-dependent pathway. However, further studies should clarify whether additional TLR-dependent or -independent pathways also exist in regulating the full spectrum of MIP action on macrophage activation.</p>
},
  year = {2012},
  journal = {Vaccine},
  volume = {30},
  pages = {5748-54},
  issn = {1873-2518},
  doi = {10.1016/j.vaccine.2012.07.002},
  language = {eng},
}