The Locus of Heat Resistance Confers Resistance to Chlorine and Other Oxidizing Chemicals in Escherichia coli.

Some chlorine-resistant isolates harbor the locus of heat resistance (LHR), a genomic island conferring heat resistance. In this study, the protective effect of the LHR for cells challenged by chlorine and oxidative stress was quantified. Cloning of the LHR protected against NaClO (32 mM; 5 min), HO (120 mM; 5 min), and peroxyacetic acid (105 mg/liter; 5 min) but not against 5.8 mM KIO, 10 mM acrolein, or 75 mg/liter allyl isothiocyanate. The lethality of oxidizing treatments for LHR-negative strains of was about 2 log CFU/ml higher than that for LHR-positive strains of The oxidation of cytoplasmic proteins and membrane lipids was quantified with the fusion probe roGFP2-Orp1 and the fluorescent probe BODIPY, respectively. The fragment of the LHR coding for heat shock proteins protected cytoplasmic proteins but not membrane lipids against oxidation. The middle fragment of the LHR protected against the oxidation of membrane lipids but not of cytoplasmic proteins. The addition of HO, NaClO, and peroxyacetic acid also induced green fluorescent protein (GFP) expression in the oxidation-sensitive reporter strain O104:H4 Δ:::: Cloning of pLHR reduced phage induction in O104:H4 Δ:::: after treatment with oxidizing chemicals. Screening of 160 strains of Shiga toxin-producing (STEC) revealed that none of them harbors the LHR, additionally suggesting that the LHR and Stx prophages are mutually exclusive. Taking our findings together, the contribution of the LHR to resistance to chlorine and oxidative stress is based on the protection of multiple cellular targets by different proteins encoded by the genetic island. Chlorine treatments are used in water and wastewater sanitation; the resistance of to chlorine is thus of concern to public health. We show that a genetic island termed the locus of heat resistance (LHR) protects not only against heat but also against chlorine and other oxidizing chemicals, adding to our knowledge of the tools used by to resist stress. Specific detection of the oxidation of different cellular targets in combination with the cloning of fragments of the LHR provided insight into mechanisms of protection and demonstrated that different fragments of the LHR protect different cellular targets. In , the presence of the LHR virtually always excluded other virulence factors. It is tempting to speculate that the LHR is maintained by strains of with an environmental lifestyle but is excluded by pathogenic strains that adapted to interact with vertebrate hosts.