Project description:Mycoplasma bovis is one of the major causative pathogens of the bovine respiratory complex disease that is characterized by enzootic pneumonia, mastitis, pleuritis and polyarthritis. M. bovis enters and colonizes the bovine respiratory epithelia through inhalation of aerosol from contaminated air. The nature of the interaction between M. bovis and bovine innate immune system is not well understood. We hypothesized that M. bovis invades blood monocytes and regulates cellular function to support its persistence and systemic dissemination. We used bovine-specific peptide kinome arrays to identify cellular signaling pathways that could be relevant to M. bovis-monocyte interaction in vitro. We validated these pathways using functional, protein and gene expression arrays. Here we show that infection of blood monocytes with M. bovis delays spontaneous or TNF-α/staurosporine-driven apoptosis, activates NF-κβ p65 subunit and inhibits caspase-9 activity. We also report that M. bovis infected bovine monocytes do not produce IFN-γ and TNF-α, although production of IL-10 is elevated. Our findings suggest that M. bovis takes over the cellular machinery of bovine monocytes to prolong bacterial survival and to possibly facilitate subsequent systemic distribution.
