Abstract
Oxidative stress is one of the major methods of microbial population control and pathogen clearing by the mammalian immune system. The methods by which bacteria are able to escape damage by host-derived oxidants such as hydrogen peroxide (H(2)O(2)) and hypochlorous acid (HOCl) have been relatively well described, while other oxidants' effects on bacteria and their genetic responses are not as well understood. Hypothiocyanite/hypothiocyanous acid (OSCN(-)/HOSCN) is one such oxidative stress agent. In this study, we used RNA-sequencing to characterize the global transcriptional response of Escherichia coli to treatment with HOSCN and the impact of deletions of the HOSCN resistance proteins RclA (HOSCN reductase), RclB, and RclC on that response. The HOSCN response of E. coli was different from the previously characterized responses of E. coli to other oxidants such as H(2)O(2), superoxide, or HOCl and distinct from the reported responses of other bacteria such as Streptococcus pneumoniae and Pseudomonas aeruginosa to HOSCN. Strikingly, deletion of any one of the Rcl proteins had very similar effects on the transcriptional response to HOSCN, indicating that any disruption of HOSCN defense in E. coli results in similar impacts, despite the fact that we do not currently understand the mechanism(s) by which RclB and RclC contribute to that defense. IMPORTANCE: Understanding how bacteria sense and respond to oxidative stress provides insights into how our bodies interact with the microbial population within us. In this study, we have characterized the genetic response of E. coli to the important immune oxidant hypothiocyanite and investigated the role of rclABC genes in that response.