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Infection and Immunity, October 2008, p. 4405-4413, Vol. 76, No. 10
0019-9567/08/$08.00+0 doi:10.1128/IAI.00575-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Department of Toxicology, Zhejiang University School of Public Health, Hangzhou, Zhejiang, 310058, China,1 The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310008, China,2 National Key Laboratory for Infectious Disease Diagnosis and Therapy, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310008, China,3 Zhejiang California International NanoSystems Institute, Hangzhou, Zhejiang, 310030, China4
Received 11 May 2008/ Returned for modification 13 June 2008/ Accepted 16 July 2008
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 of M. 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-cytochrome c reductase complex core protein I mitochondrial precursor. The oxidative status of M. pneumoniae-infected cells was evaluated, and the results revealed that M. pneumoniae infection indeed caused generation of reactive oxygen species (ROS). It was further shown that M. pneumoniae infection also induced DNA double-strand breaks, as demonstrated by the formation of
H2AX foci. On the other hand, an ROS scavenger, N-acetylcysteine, could inhibit the ROS generation, as well as decrease
H2AX focus formation. This is the first report showing that M. 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 of M. pneumoniae.
Published ahead of print on 28 July 2008.
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