期刊
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2021.669168
关键词
tuberculosis; mesenchymal stem cell; NOD-2; TLR-4; autophagy
资金
- Council of Scientific and Industrial Research (CSIR), India
- Department of Science and Technology (DST)
- Indian Council of Medical Research (ICMR)
- University Grant Commission
- CSIR
The study observed that MSC stimulated through TLR-4 and NOD-2 (N2.T4) activated MSC and augmented the secretion of pro-inflammatory cytokines, co-localized Mtb in the lysosomes, induced autophagy, enhanced NF-kappa B activity via p38 MAPK signaling pathway, and significantly reduced the intracellular survival of Mtb in the MSC. Overall, the results suggest that triggering through N2.T4 may be a future method of immunotherapy to eliminate the Mtb concealed inside the MSC.
For a long time, tuberculosis (TB) has been inflicting mankind with the highest morbidity and mortality. Although the current treatment is extremely potent, a few bacilli can still hide inside the host mesenchymal stem cells (MSC). The functional capabilities of MSCs are known to be modulated by TLRs, NOD-2, and RIG-1 signaling. Therefore, we hypothesize that modulating the MSC activity through TLR-4 and NOD-2 can be an attractive immunotherapeutic strategy to eliminate the Mtb hiding inside these cells. In our current study, we observed that MSC stimulated through TLR-4 and NOD-2 (N2.T4) i) activated MSC and augmented the secretion of pro-inflammatory cytokines; ii) co-localized Mtb in the lysosomes; iii) induced autophagy; iv) enhanced NF-kappa B activity via p38 MAPK signaling pathway; and v) significantly reduced the intracellular survival of Mtb in the MSC. Overall, the results suggest that the triggering through N2.T4 can be a future method of immunotherapy to eliminate the Mtb concealed inside the MSC.
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