Abstract
Vibrio vulnificus is a causative agent of fatal septicemia and necrotic wound infection and the pathogen infection became an important public health problem in many counties. Vibrio vulnificus causes RtxA1 toxin-induced acute cell death. We tried to identify natural products that inhibit the acute cytotoxicity of V. vulnificus using a lactate hydrogenase assay. A polyphenol pyrogallol protected HeLa cells from V. vulnificus-induced cytotoxicity. Pyrogallol also decreased the growth of V. vulnificus; this inhibitory effect was more significant during log phase than stationary phase. To further elucidate the inhibitory mechanism, pyrogallol-induced toxicity was compared between a V. vulnificus catalase-peroxidase mutant (katG−) and the isogenic wild-type MO6-24/O strains. No growth was observed for the katG− mutant in the presence of pyrogallol (50 μg/mL) even after 24 h, whereas the wild-type strain demonstrated growth recovery following a prolonged lag phase. Pyrogallol-mediated growth inhibition of the katG− mutant strain was partially rescued by exogenous catalase treatment. These results indicate that the mechanism by which pyrogallol inhibits the growth and cytotoxicity of V. vulnificus likely involves polyphenol-induced prooxidant damage. Taken together, these results suggest that pyrogallol has potential for development as a new paradigm drug to treat infectious diseases.
Highlights
Vibrio vulnificus is a halophilic, estuarine bacterium that causes fatal septicemia and necrotic wound infections [1, 2]
Live V. vulnificus is highly toxic to host cells; this cytotoxicity is caused mainly by the repeats-in-toxin A1 (RtxA1) toxin [5]
The inhibitory effect of pyrogallol on V. vulnificus cytotoxicity was quantified using the Lactate dehydrogenase (LDH) assay, which demonstrated that pyrogallol significantly inhibited the cytotoxicity (Fig 1B)
Summary
Vibrio vulnificus is a halophilic, estuarine bacterium that causes fatal septicemia and necrotic wound infections [1, 2]. V. vulnificus infection exhibits a broad pathogenic spectrum, a fulminating course, and a high mortality rate (> 50%) with death occurring within days [3]. This pathogen represents a good model organism for the study of bacterial septicemia. We have reported that the major virulence factor of V. vulnificus is repeats-in-toxin A1 (RtxA1), which induces the programmed necrotic death of host cells [5,6,7].
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