Staphylococcus Epidermidis Lipoteichoic Acid: Exocellular Release And Ltas Gene Expression In Clinical And Commensal Isolates

JOURNAL OF MEDICAL MICROBIOLOGY(2017)

引用 9|浏览14
暂无评分
摘要
Purpose. Staphylococcus epidermidis ATCC12228 lipoteichoic acid (LTA) inhibits TNF alpha production from keratinocytes that are activated with poly I:C. However, this effect has not been proven in clinical or commensal isolates.Methodology. The <10 kDa fractions of S. epidermidis isolates from ocular infections (n=56), healthy skin (n=35) and healthy conjunctiva (n=32) were obtained. TNF alpha production was determined by ELISA in HaCaT keratinocytes stimulated with poly I: C and with the <10 kDa fractions. LTA in the cytoplasmic membrane and in the <10 kDa fractions of the isolates was determined during bacterial growth by flow cytometry, Western blot and electrospray ionization mass spectrometry. The expression levels of ugtP, ltaA and ltaS were evaluated.Results. Two populations of isolates were found: a population that inhibited TNF alpha production (TNF alpha-inhibitor isolates) and a population that did not inhibit it (TNF alpha non-inhibitor isolates). The cells from the TNF alpha-inhibitor isolates had less LTA in the cytoplasmic membrane compared to the cells from the TNF alpha non-inhibitor isolates (P<0.05). Similarly, LTA was detected in the supernatants of TNF alpha-inhibitor isolates, and it was absent in TNF alpha non-inhibitor isolates. High expression levels of the ugtP and ltaA genes in the 1850I (TNF alpha-inhibitor isolate) and 37HS (TNF alpha non-inhibitor isolate) isolates were found during bacterial growth. However, the ltaS gene had a low expression level (P<0.05) in the 37HS isolate.Conclusion. The TNF alpha-inhibitor isolates release LTA due to high expression of the LTA synthesis genes. By contrast, TNF alpha non-inhibitor isolates do not release LTA due to low expression level of the ltaS gene.
更多
查看译文
关键词
Staphylococcus epidermidis,LTA,keratinocyte,TNFalpha,ltaS
AI 理解论文
溯源树
样例
生成溯源树,研究论文发展脉络
Chat Paper
正在生成论文摘要