Yanan Li, Zhongjia Jiang, Di Xue, Guangcun Deng, Min Li, Xiaoming Liu, Yujiong Wang

Mycoplasma ovipneumoniae (M. ovipneumoniae) is a species of Mycoplasma bacteria that specifically infects sheep and goat, causing ovine infectious pleuropneumonia. However, the mechanism underlying the pathogen-host interaction between M. ovipneumoniae and airway epithelial cells is unknown. A primary air-liquid interface (ALI) epithelial culture model generated from the bronchial epithelial cells of Ningxia Tan sheep (ovis aries) was employed to explore the potential mechanism of M. ovipneumoniae-induced cell apoptosis by characterizing the production of reactive oxygen species (ROS), methane dicarboxylic aldehyde (MDA) and anti-oxidative enzymes, as well as the mitochondrial membrane potentials, cytochrome C release, and activities of ERK and caspase signalling pathways. Increased ROS production and MDA concentration with mitochondrial membrane dysfunction and apoptotic cell death but decreased expression of the antioxidant enzymes catalase (CAT), glutathione synthetase (GSS), total superoxide dismutaes (T-SOD) and Mn-SOD were observed in sheep airway epithelial cells infected with M. ovipneumoniae. Mechanistically, the M. ovipneumoniae-induced cell apoptosis and disruption of mitochondrial integrity reflected mechanisms by which pathogen-activated mitogen-activated protein kinase (MAPK) signalling sequentially led to mitochondrial damage and release of Cyt-C into the cytoplasm, which in turn triggered the activation of caspase signalling cascade, resulting in the apoptosis of host cells. These results suggest that M. ovipneumoniae-induced ROS and MAPK signalling-mediated mitochondrial apoptotic pathways might play key roles in the pathogenesis of M. ovipneumoniae infection in sheep lungs.