小桶
发病机制
信号转导
免疫学
失调
慢性阻塞性肺病
微生物群
生物
先天免疫系统
恶化
基因表达
微生物学
医学
基因
免疫系统
生物信息学
内科学
遗传学
转录组
作者
Yao Li,Xiaoyan Mao,Pengfei Shi,Zongren Wan,Dan Yang,Ting Ma,Baolan Wang,Jipeng Wang,Jingjing Wang,Rong Zhu
标识
DOI:10.3389/fcimb.2024.1386201
摘要
Objective To explore the underlying mechanisms the airway microbiome contributes to Acute Exacerbation of Chronic Obstructive Pulmonary Disease(AECOPD). Methods We enrolled 31 AECOPD patients and 26 stable COPD patients, their sputum samples were collected for metagenomic and RNA sequencing, and then subjected to bioinformatic analyses. The expression of host genes was validated by Quantitative Real-time PCR(qPCR) using the same batch of specimens. Results Our results indicated a higher expression of Rothia mucilaginosa ( p =0.015) in the AECOPD group and Haemophilus influenzae ( p =0.005) in the COPD group. The Different expressed genes(DEGs) detected were significantly enriched in "type I interferon signaling pathway"( p <0.001, q =0.001) in gene function annotation, and "Cytosolic DNA-sensing pathway"( p =0.002, q =0.024), "Toll-like receptor signaling pathway"( p =0.006, q =0.045), and "TNF signaling pathway"( p =0.006, q =0.045) in KEGG enrichment analysis. qPCR amplification experiment verified that the expression of OASL and IL6 increased significantly in the AECOPD group. Conclusion Pulmonary bacteria dysbiosis may regulate the pathogenesis of AECOPD through innate immune system pathways like type I interferon signaling pathway and Toll-like receptor signaling pathway.
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