Oxidation-sensing Regulator AbfR Regulates Oxidative Stress Responses, Bacterial Aggregation, and Biofilm Formation in Staphylococcus epidermidis

Xing Liu1, Xiaoxu Sun1, Youcong Wu2, Cen Xie1, Wenru Zhang1, Dan Wang3, Xiaoyan Chen1, Di Qu2, Jianhua Gan2, Hao Chen3, Hualiang Jiang1, Lefu Lan1 and Cai-Guang Yang1,*

Staphylococcus epidermidis is a notorious human pathogen that is the major cause of infections related to implanted medical devices. Although redox regulation involving reactive oxygen species (ROS) is now recognized as a critical component of bacterial signaling and regulation, the mechanism by which S. epidermidis senses and responds to oxidative stress remains largely unknown. Here, we report a new oxidation-sensing regulator, AbfR (Aggregation and Biofilm Formation Regulator) in S. epidermidis. An environment of oxidative stress mediated by hydrogen peroxide (H2O2) or cumene hydroperoxide (CHP) markedly up-regulates the expression of abfR gene. Similar to Pseudomonas aeruginosa OspR, AbfR is negatively auto-regulated and dissociates from promoter DNA in the presence of oxidants. In vivo and in vitro analyses indicate that Cys-13 and Cys-116 are the key functional residues to form an intersubunit disulphide bond upon oxidation in AbfR. We further show that deletion of abfR leads to a significant induction in H2O2 or CHP resistance, enhanced bacterial aggregation, and reduced biofilm formation. These effects are mediated by de-repression of SERP2195 and gpxA-2 that lie immediately downstream of the abfR gene in the same operon. Thus, oxidative stress likely acts as a signal to modulate S. epidermidis key virulence properties through AbfR.

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