Pathogenicity analysis of a tyrosine kinase Cps2C mutant strain of Streptococcus suis serotype 2
This study was aimed at predicting the biological function of Streptococcus suis serotype 2(S.suis 2)tyrosine kinase Cps2C through bioinformatics and analyzing its effects on S.suis 2 pathogenicity.Online bioinformatics tools were used to analyze and predict the localization,conserved domains,transmembrane domains,protein similarity,and protein three-di-mensional structure of Cps2C.A BALB/c mouse infection model was used to compare and analyze clinical characteristics,mor-tality rates,and blood bacterial loads in mice infected with the wild-type strain 05ZYH33 and the cps2C gene knockout strainΔcps2C.Additionally,heart,brain,and joint tissue sections from infected mice were stained with hematoxylin and eosin(HE)for comparative pathological analysis.The Cps2C protein-coding gene is located upstream of the capsule biosynthesis locus cps,lacks transmembrane domains,is a homologous protein to Streptococcus pneumoniae tyrosine kinase CpsD with a 64％amino acid sequence similarity,and is potentially involved in bacterial capsule synthesis regulation.Cps2C deficiency significantly de-creased the pathogenicity of S.suis 2 in mice(P＜0.05).Compared with the wild-type strain,the Δcps2C strain showed a sig-nificantly lower blood bacterial load(P＜0.000 1).Heart,brain,and joint tissues of mice infected intraperitoneally with strains 05ZYH33 and Δcps2C remained structurally intact without e-dema,hemorrhage,or inflammatory cell infiltration;moreo-ver,characteristic lesion features of endocarditis,meningitis,or arthritis were absent.Streptococcus suis serotype 2 tyrosine kinase Cps2C may be an important regulatory factor in capsule biosynthesis,and its deficiency decreases bacterial blood survival capability and pathogenicity in mice.
Streptococcus suis serotype 2tyrosine kinaseCps2Cpathogenicitycapsule
万方数据
维普
