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Research Paper

Contribution of nuclease to the pathogenesis of Aeromonas hydrophila

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Pages 515-522 | Received 26 Jan 2015, Accepted 04 May 2015, Published online: 24 Jun 2015
 

Abstract

Aeromonas hydrophila is a gram-negative bacterium that is widely distributed in aquatic environments and can cause septicemia in both fish and humans. However, the underlying mechanisms leading to severe infection are not well understood. In this study, an A. hydrophila nuclease (ahn) deletion mutant was constructed to investigate its contribution to pathogenesis. This mutant did not differ from the wild-type strain in terms of its growth or hemolytic phenotype. However, the ahn-deficient mutant was more susceptible to being killed by fish macrophages and mouse blood in vitro. Furthermore, evidence obtained using both fish and murine infection models strongly indicated that the inactivation of Ahn impaired the ability of A. hydrophila to evade innate immune clearance in vivo. More importantly, the virulence of the mutant was attenuated in both fish and mice, with reductions in dissemination capacities and mortality rates. These findings implicate Ahn in A. hydrophila virulence, with important functions in evading innate immune defenses.

This article refers to:
Aeromonas hydrophila virulence

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Acknowledgments

We thank Prof. Lu Chengping and Prof. Liu Yongjie at Nanjing Agricultural University for generously providing the A. hydrophila J-1 strain.

Funding

This work was jointly supported by the Natural Science Foundation of China (31402341, 31372563), China Postdoctoral Science Foundation (2014M550400), State Key Laboratory of Freshwater Ecology and Biotechnology Open Foundation (2015FB05), Natural Science Foundation of Hubei Province (2015CKC901), Fundamental Research Funds for the Central Universities (2013PY069, 2014PY035) and the Huazhong Agricultural University Scientific & Technological Self-innovation Foundation (52204–12020).

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