| First Author | Kumar P | Year | 2019 |
| Journal | BMC Res Notes | Volume | 12 |
| Issue | 1 | Pages | 648 |
| PubMed ID | 31590685 | Mgi Jnum | J:290608 |
| Mgi Id | MGI:6435410 | Doi | 10.1186/s13104-019-4679-0 |
| Citation | Kumar P, et al. (2019) Mycobacterium indicus pranii therapy induces tumor regression in MyD88- and TLR2-dependent manner. BMC Res Notes 12(1):648 |
| abstractText | OBJECTIVES: Mycobacterium indicus pranii (MIP) is an atypical mycobacterium species with potent antitumor efficacy. Macrophages and dendritic cells (DCs) are antigen-presenting cells, playing key roles in the activation of antitumor immunity. We have previously shown the potent activation of macrophages and DCs by MIP, which is mediated by MyD88-TLR2 signaling axis. In the present study, we further examined the role of MyD88 and TLR2 in MIP-mediated tumor regression. RESULTS: Wild-type and MyD88(-/-) mice were implanted with B16F10 tumor cells, treated with MIP or phosphate-buffered saline (PBS) and monitored for tumor growth. As expected, MIP therapy led to significant tumor regression in wild-type mice. However, antitumor efficacy of MIP was lost in MyD88(-/-) animals. Both PBS-treated (control) and MIP-treated MyD88(-/-) mice developed tumors with comparable volume. Since MyD88 relays TLR engagement signals, we analyzed the antitumor efficacy of MIP in TLR2(-/-) and TLR4(-/-) mice. It was observed that MIP therapy reduced tumor burden in wild-type and TLR4(-/-) mice but not in TLR2(-/-) mice. Tumor volume in MIP-treated TLR2(-/-) mice were comparable with those in PBS-treated wild-type animals. These results implicated the MyD88-TLR2 signaling axis in the antitumor efficacy of MIP. |
