PM2.5是大气污染物中导致哮喘的关键成分，其中菌群（细菌、病毒、真菌）等生物性污染物含量占25%。菌群的生长繁殖与温湿度等气候因素密切相关，随呼吸进入人体，部分菌群得以定植并引起疾病发生。广州作为南亚热带海洋性气候城市，其PM2.5中菌群的分布、特征和致病性并不完全清楚。本课题通过环境卫生学、宏基因组与比较基因组学、免疫学和病原生物学方法，分析广州大气PM2.5、土壤、动物和哮喘患者呼吸道中的菌群差异，发现可定植呼吸道的特异菌群；并以模式识别受体TLR识别菌群相关分子模式从而诱导TSLP导致哮喘通路为核心，通过荧光素酶报告基因、定量PCR、Crisper/Cas9等方法寻找可激活TLR/TSLP的菌群或毒力因子；利用TSLP基因敲除小鼠和哮喘模型小鼠研究菌群的致哮喘作用以及抗菌群血清的防治作用，为揭示广州地区PM2.5的致病作用提出新机制，并为发明PM2.5所致哮喘的防治方法提供新思路。

PM2.5 is the key component of the air pollutant in causing the asthma. Biological pollutants in air pollutants, including bacteria, viruses, fungi, etc. accounted for 25%. The growth and propagation of the microbiota is closely related to the climatic factors such as temperature and humidity, which can enter and colonize in the human body with the breath and cause disease.Guangzhou is a subtropical marine climate city, in which the distribution, characteristics and pathogenicity of microbiota in PM2.5 are not fully understood.We adopt a multi-disciplinary research and combine environmental hygiene, metagenomic and comparative genomic science, immunology and pathogenic biology methods to analysis the microbiota differences among PM2.5, soil, repiratory tract among animals and asthma patients in Guanghzou, in order to find out specific microbiota that can colonize in the repiratory tract. The key pathway is that TLR, a pattern recognition receptor, can recognize the microbiota and induce TSLP, which lead to asthma. We aim to find the specific microbiota or virulence factors, which can activate TLR/TSLP pathway, using luciferase report gene, quantitative PCR, Crisper/Cas9 etc. methods. At last, TSLP gene knockout mice and asthma model mice are used to study the roles of microbiota in causing asthma and antibacterial effects of serogroup in the prevention and treatment of asthma.Our research will reveal the new pathogenic mechanism of PM2.5 and provide a new idea for the prevention and treatment of asthema caused by PM2.5 in Guangzhou.