Generation of reactive oxygen species by lethal attacks from competing microbes

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 112; no. 7; pp. 2181 - 2186
• Main Authors: Dong, Tao G., Dong, Shiqi, Catalano, Christy, Moore, Richard, Liang, Xiaoye, Mekalanos, John J.
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 17.02.2015; National Acad Sciences
• Subjects: Antibiotics; Apoptosis; Bacteriophages - physiology; Biological Sciences; Cells; E coli; Escherichia coli; Humans; Microscopy, Fluorescence; Molecules; Nonnative species; Polymerase Chain Reaction; Reactive Oxygen Species - metabolism; Vibrio cholerae - virology; Viruses; interspecies competition; phage; T6SS; antibiotics; reactive oxygen species
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.1425007112

Significance How microbes respond to lethal attacks from competing species is not fully understood. Here, we investigated the response of Escherichia coli to attacks from the type VI secretion system (T6SS), bacteriophage P1 vir , and polymyxin B. We report that generation of reactive oxygen species (ROS) is a general outcome of potentially lethal activities mediated by contact-dependent or contact-independent interactions of aggressive competing bacterial species and phage. An ROS response gene, soxS , is highly induced in response to all sources of attacks tested. This discovery will likely prompt other investigations into why evolution has selected expression of this gene as a “first responder” to potentially lethal interspecies competition. Whether antibiotics induce the production of reactive oxygen species (ROS) that contribute to cell death is an important yet controversial topic. Here, we report that lethal attacks from bacterial and viral species also result in ROS production in target cells. Using soxS as an ROS reporter, we found soxS was highly induced in Escherichia coli exposed to various forms of attacks mediated by the type VI secretion system (T6SS), P1 vir phage, and polymyxin B. Using a fluorescence ROS probe, we found enhanced ROS levels correlate with induced soxS in E. coli expressing a toxic T6SS antibacterial effector and in E. coli treated with P1 vir phage or polymyxin B. We conclude that both contact-dependent and contact-independent interactions with aggressive competing bacterial species and viruses can induce production of ROS in E. coli target cells.