A methionine sulfoxide reductase A homolog gene(msrA1)deficiency significantly attenuates the virulence of Nocardia seriolae.

Abstract

Nocardia seriolae, a facultative intracellular pathogenic actinobacteria, is the primary aetiological agent of nocardiosis in both freshwater and marine fish. Methionine sulfoxide reductases (Msrs) has been shown to play important role in defensing against oxidative stress in many pathogenic bacteria. In present study, a methionine sulfoxide reductase A homolog gene (msrA1) was identified in the genome of N. seriolae and the gene deficient strain ΔmsrA1 was generated by homogenous recombination method. Growth curve showed the viable counts of ΔmsrA1 was significant more than its wild type (WT) stain during stationary phase. Compare with the WT strain, ΔmsrA1 showed significant more sensitive to hydrogen peroxide, but exhibited almost the same enduring ability to sodium hypochlorite. In a fish head kidney cell line (LYC-hK) model, the ΔmsrA1 strain displayed significantly decreased survival rates, alongside the weaken reactive oxygen species (ROS) and apoptosis inducing capacity, compare with its parental strain. Using largemouth bass as the infection model, the ΔmsrA1 strain showed significantly decreased bacterial loads in tissues and attenuated virulence, compare with the WT strain. Given the above, msrA1 was shown to be implicated in virulence of N. seriolae via enhancing the ability to resist the in vivo oxidative stress and survive inside host.