title: capB2Expression Is Associated withStaphylococcus aureusPathogenicity.
abstract: CapB2 is recognized as a tyrosine kinase and is likely a vital factor in extracellular polysaccharide synthesis inStaphylococcus aureus, but its pathogenicity function and regulatory mechanism remain obscure. Here, we demonstrate that CapB2 enhances bacterial virulence in a murine model. Mice infected with the wild type SA75 strain exhibited significantly larger (P< 0.05) skin lesions from days 4 to 7 of infection than those challenged with thecapB2mutant strain. The effect on virulence was reverted by restoring thecapB2mutation to the wild type. The related components of the wild type SA75 cell wall in thecapB2mutant strain (SA75ΔcapB2) were thinner than wild type SA75 strain and thecapB2mutant complemented strain (SA75ΔcapB2-C), which was determined by the transmission electron microscopy. The survival percentages of the wild type strain SA75 and SA75ΔcapB2-C were significantly higher relative to SA75ΔcapB2. The results of qRT-PCR studies also indicated that mutations in regulatory genesarAled to a drastic increase in capB2 gene transcription, with a 326-fold increase of growth at 6 h compared with the wild type strain, suggesting that sarA is a major negative regulator of capB2 expression. Taken together, these results demonstrate that the expression of CapB2 promotesS. aureusvirulence in a mouse model of skin infection, and thatcapB2gene transcription is regulated negatively by SarA.
authors.affiliation: Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Li
authors.affiliation: Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Yinjuan
authors.initials: Y
authors.lastname: Guo
authors.affiliation: Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Shanshan
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Jingnan
authors.initials: J
authors.lastname: Lv
authors.affiliation: Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Xiuqin
authors.initials: X
authors.lastname: Qi
authors.affiliation: Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Zengqiang
authors.initials: Z
authors.lastname: Chen
authors.affiliation: Department of Clinical Microbiology, Ruijin Hospital of Shanghai Jiaotong University Shanghai, China.
authors.forename: Lizhong
authors.initials: L
authors.lastname: Han
authors.affiliation: Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Xueqing
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Respiratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Liangxing
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Laboratory Medicine, the First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.
authors.forename: Fangyou
authors.initials: F
authors.lastname: Yu
keywords: Staphylococcus aureus; capB2; regulation; sarA; virulence factor