12月14日 张凌娟:Age-related loss of innate immune antimicrobial function of dermal fat is mediated by TGF


报告题目:Age-related loss of innate immune antimicrobial function of dermal fat is mediated by TGF
报告人:张凌娟 教授,厦门大学药学院
主持人:赖玉平 教授
报告时间:2018年12月14日 14:00
报告地点:生命科学学院534小会议室
 
报告人简介:张凌娟博士,2009年获得美国俄勒冈州立大学博士学位,2009至2014在美国加州大学圣地亚哥分校作博士后,2014年升任为项目科学家,2018年受聘为厦门大学药学院教授。在美国有近15年分子生物学和基础医学研究的学习和研究经历,在皮肤医学专项领域也有近10年的研究经验, 迄今发表论著20余篇。在皮肤天然免疫机制及调控领域开展了一系列独创性的研究工作,发现脂肪前体细胞可通过大量释放多肽抗生素来抵御细菌感染,这种抗菌多肽还参与银屑病的调控, 上述研究成果以第一作者身份在Science、Immunity 和Current Biology等国际顶级学术期刊上,多次受邀在国际学术会议上做学术报告。在UCSD期间以PI身份主持美国国立卫生研究院(NIH) RO1研究课题(2百万美金/5年)。
 
报告摘要: Dermal fibroblasts (dFB) resist infection by locally differentiating into adipocytes and producing the antimicrobial peptide cathelicidin in response to S. aureus. Here we show that neonatal skin has abundant adipogenic dFB and express high levels cathelicidin in dermal fat. The pool of adipogenic and antimicrobial dFB declines after birth, leading to an age-dependent loss of dermal fat and a decrease of adipogenesis and Camp production in response to infection. TGFβ was identified as a key upstream regulator of this process that acts on uncommitted embryonic and adult dFB, and inhibits the adipogenic and antimicrobial function of dFB. Furthermore, inhibition of the TGFβ receptor restored the adipogenic and antimicrobial function of dFB in culture and increased resistance of adult mice to S. aureus infection. These results provide new insight into changes in the skin innate immune system that occur between the perinatal and adult periods of life.