Identification of the <Emphasis Type="Italic">Vibrio vulnificus ahpC</Emphasis>l gene and its influence on survival under oxidative stress and virulence |
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Authors: | Woon Ki Baek Hyun Sung Lee Man Hwan Oh Myung Jin Koh Kun-Soo Kim Sang Ho Choi |
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Institution: | (1) Department of Internal Medicine B, University of Greifswald, Friedrich-Loeffler-Strasse 23, 17489 Greifswald, Germany;(2) Loeffler Institute for Medical Microbiology, University of Greifswald, Martin-Luther-Strasse 6, 17489 Greifswald, Germany;(3) Department of Surgery, University of Greifswald, Friedrich-Loeffler-Strasse 23, 17489 Greifswald, Germany;(4) Institute of Pathology, University of Greifswald, Friedrich-Loeffler-Strasse 23, 17489 Greifswald, Germany |
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Abstract: | Pathogens have evolved sophisticated mechanisms to survive oxidative stresses imposed by host defense systems, and the mechanisms
are closely linked to their virulence. In the present study, ahpCl, a homologue of Escherichia coli ahpC encoding a peroxiredoxin, was identified among the Vibrio vulnificus genes specifically induced by exposure to H2O2. In order to analyze the role of AhpCl in the pathogenesis of V. vulnificus, a mutant, in which the ahpCl gene was disrupted, was constructed by allelic exchanges. The ahpCl mutant was hypersusceptable to killing by reactive oxygen species (ROS) such as H2O2 and t-BOOH, which is one of the most commonly used hydroperoxides in vitro. The purified AhpCl reduced H2O2 in the presence of AhpF and NADH as a hydrogen donor, indicating that V. vulnificus AhpCl is a NADH-dependent peroxiredoxin and constitutes a peroxide reductase system with AhpF. Compared to wild type, the
ahpCl mutant exhibited less cytotoxicity toward INT-407 epithelial cells in vitro and reduced virulence in a mouse model. In addition, the ahpCl mutant was significantly diminished in growth with INT-407 epithelial cells, reflecting that the ability of the mutant to
grow, survive, and persist during infection is also impaired. Consequently, the combined results suggest that AhpCl and the
capability of resistance to oxidative stresses contribute to the virulence of V. vulnificus by assuring growth and survival during infection. |
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