Mycoplasma bovis delay in apoptosis of macrophages is accompanied by increased expression of anti-apoptotic genes, reduced cytochrome C translocation and inhibition of DNA fragmentation.

Bacterial pathogens have evolved to manipulate host cell death and survival pathways for their intracellular persistence. Understanding the ability of a bacterium to induce or inhibit cell death is essential for elucidating the disease pathogenesis and suggesting potential therapeutic options to manage the infection. In recent years, apoptosis inhibition by different bacteria has been suggested as a mechanism of survival by allowing the pathogen to replicate and disseminate in the host. Mycoplasma bovis has evolved mechanisms to invade and modulate apoptosis of bovine peripheral blood mononuclear cells (PBMC), red blood cells (RBCs), primary macrophages and monocytes. To date, these mechanisms are poorly understood. Using apoptosis assays such as Annexin V binding, caspases activity, reactive oxygen species production, DNA fragmentation and differential gene expression we set out to determine how M. bovis modulates macrophage survival. Using the BoMac cell line, we report a significant reduction in STS-induced apoptosis through caspase dependent manner. Besides activating the NF-kβ pathway and inhibiting caspases 3, 6 and 9, M. bovis strain Mb1 also inhibits production of reactive oxygen species and DNA fragmentation of the host cell. We also report a significant up-regulation of the anti-apoptotic genes Bcl-2 and Bcl-X upon infection. Our results indicate that M. bovis strain Mb1 inhibits the intrinsic pathway of apoptosis and up-regulate survival genes in BoMac cells.