Department of Respiratory and Critical Care Medicine, Huaian Clinical College of Xuzhou Medical University, Huaian, China.
Department of Intensive Care Unit, The Affiliated Huaian Hospital of Xuzhou Medical University, Huaian, China.
Front Cell Infect Microbiol. 2024 Jul 18;14:1386201. doi: 10.3389/fcimb.2024.1386201. eCollection 2024.
To explore the underlying mechanisms the airway microbiome contributes to Acute Exacerbation of Chronic Obstructive Pulmonary Disease(AECOPD).
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.
Our results indicated a higher expression of (=0.015) in the AECOPD group and (=0.005) in the COPD group. The Different expressed genes(DEGs) detected were significantly enriched in "type I interferon signaling pathway"(<0.001, =0.001) in gene function annotation, and "Cytosolic DNA-sensing pathway"(=0.002, =0.024), "Toll-like receptor signaling pathway"(=0.006, =0.045), and "TNF signaling pathway"(=0.006, =0.045) in KEGG enrichment analysis. qPCR amplification experiment verified that the expression of and increased significantly in the AECOPD group.
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.
探索气道微生物组在慢性阻塞性肺疾病急性加重（AECOPD）中的作用机制。
我们招募了 31 名 AECOPD 患者和 26 名稳定期 COPD 患者，收集他们的痰标本进行宏基因组和 RNA 测序，并进行生物信息学分析。使用相同批次的标本通过定量实时 PCR(qPCR)验证宿主基因的表达。
我们的结果表明，AECOPD 组的表达较高（=0.015），COPD 组的表达较高（=0.005）。检测到的差异表达基因（DEGs）在基因功能注释中显著富集于“I 型干扰素信号通路”（<0.001，=0.001），KEGG 富集分析中还显著富集于“胞质 DNA 感应途径”（=0.002，=0.024）、“Toll 样受体信号通路”（=0.006，=0.045）和“TNF 信号通路”（=0.006，=0.045）。qPCR 扩增实验验证了 AECOPD 组中表达显著增加。
肺部细菌失调可能通过 I 型干扰素信号通路和 Toll 样受体信号通路等先天免疫系统途径调节 AECOPD 的发病机制。
