Mycoplasma pneumoniae Infection Induces Reactive Oxygen Species and DNA Damage in A549 Human Lung Carcinoma Cells

Mycoplasma pneumoniae is a frequent cause of community-acquired bacterial respiratory infections in children and adults. In the present study, using a proteomic approach, we studied the effects ofM. pneumoniae infection on the protein expression profile of A549 human lung carcinoma cells.M. pneumoniae infection induced changes in the expression of cellular proteins, in particular a group of proteins involved in the oxidative stress response, such as glucose-6-phosphate 1-dehydrogenase, NADH dehydrogenase (ubiquinone) Fe-S protein 2, and ubiquinol-cytochromec reductase complex core protein I mitochondrial precursor. The oxidative status ofM. pneumoniae -infected cells was evaluated, and the results revealed thatM. pneumoniae infection indeed caused generation of reactive oxygen species (ROS). It was further shown thatM. pneumoniae infection also induced DNA double-strand breaks, as demonstrated by the formation of γH2AX foci. On the other hand, an ROS scavenger,N -acetylcysteine, could inhibit the ROS generation, as well as decrease γH2AX focus formation. This is the first report showing thatM. pneumoniae infection can directly induce DNA damage, at least partially, through the generation of ROS, and thus this report strengthens the powerful application of proteomics in the study of the pathogenesis ofM. pneumoniae .