题　目：

The dopaminergic innervation of allergic childhood asthma

报告人：

王伟 博士（美国哈佛医学院）

主持人：

赵金存 教授

时　间：

2023年11月7日（星期二） 上午10:00 - 11:00

地　点：

广州医科大学越秀校区10号楼1306会议室

讲者介绍：

王伟，博士，2010年于吉林大学获得学士学位，2015年于北京协和医学院获得博士学位，随后前往美国哈佛医学院进行博士后培训，2022年晋升为讲师。研究方向为呼吸系统疾病的免疫学和组学研究，从免疫学角度，利用生物信息学解析急性肺损伤和过敏性哮喘的发病机制，寻找潜在药物靶点。共发表文章17篇，包括以第一作者或共同通讯作者身份发表在Immunity，Cell Research，Journal of Allergy and Clinical Immunology, eBioMedicine, American Journal of Respiratory Cell and Molecular Biology, Scientific Reports和STAR Protocols等杂志上，总引用次数超1000次。获得国家和国际发明专利各1项。作为共同负责人获得美国国立卫生院R21基金1项。担任Comparative Immunology, Microbiology & Infectious Diseases和Infectious Medicine杂志编委，Frontiers in Neuroscience和Frontiers in Cellular and Infection Microbiology杂志客座编辑。

讲座摘要：

Young children are more susceptible to developing allergic asthma than adults. As neural innervation of the peripheral tissue continues to develop after birth, neurons may modulate tissue inflammation in an age-related manner. In addition, allergic asthma develops from allergen exposure in early childhood and progresses into adulthood. The central mediator of progressive allergic asthma is allergen-specific, TH2–resident memory cells (TRMs). This talk will discuss the emerging role of dopaminergic nerves in modulating acute type 2 inflammation and recurrence of allergic asthma. Our work demonstrates that 1) sympathetic nerves underwent a dopaminergic-to-adrenergic transition during post-natal development of the lung in mice and humans; 2) Dopamine signaled through a specific dopamine receptor (DRD4) to promote TH2 cell differentiation and proliferation; 3) The dopamine-DRD4 pathway acted synergistically with the cytokine IL-4 by upregulating IL-2-STAT5 signaling and reducing inhibitory histone trimethylation at Th2 gene loci; 4) In murine models of allergen exposure, the dopamine-DRD4 pathway augmented acute Th2 inflammation in the lungs of young mice. However, this pathway operated marginally after sympathetic nerves became adrenergic in the adult lung.；5) Blockade of dopamine-DRD4 signaling following neonatal allergen exposure impairs lung residence of TH2-TRM and ameliorates anamnestic inflammation in adults. Taken together, the communication between dopaminergic nerves and CD4+ T cells provides an age-related mechanism underlying the susceptibility to allergic inflammation in the early lung and asthma recurrence in the adult lung.

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