| First Author | Bickett TE | Year | 2020 |
| Journal | Front Immunol | Volume | 11 |
| Pages | 1202 | PubMed ID | 32625209 |
| Mgi Jnum | J:311689 | Mgi Id | MGI:6728965 |
| Doi | 10.3389/fimmu.2020.01202 | Citation | Bickett TE, et al. (2020) Characterizing the BCG Induced Macrophage and Neutrophil Mechanisms for Defense Against Mycobacterium tuberculosis. Front Immunol 11:1202 |
| abstractText | The live attenuated Mycobacterium bovis strain, Bacille Calmette Guerin (BCG) is a potent innate immune stimulator. In the C57BL/6 mouse model of tuberculosis, BCG vaccination leads to a significant reduction of Mycobacterium tuberculosis burden after aerogenic infection. Our studies indicated that BCG induced protection against pulmonary tuberculosis was independent of T cells and present as early as 7 days after vaccination. This protection showed longevity, as it did not wane when conventional T cell and TNF-alpha deficient mice were infected 30 days post-vaccination. As BCG induced mycobacterial killing after 7 days, this study investigated the contributions of the innate immune system after BCG vaccination to better understand mechanisms required for mycobacterial killing. Subcutaneous BCG inoculation resulted in significant CD11b(+)F4/80(+) monocyte subset recruitment into the lungs within 7 days. Further studies revealed that killing of mycobacteria was dependent on the viability of BCG, because irradiated BCG did not have the same effect. Although others have identified BCG as a facilitator of trained innate immunity, we found that BCG reduced the mycobacterial burden in the absence of mechanisms required for trained innate immunity, highlighting a role for macrophages and neutrophils for vaccine induced killing of M. tuberculosis. |
