Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Molecular Therapy: Nucleic Acids

Guanghe Fei¹  Aiqun Xu²  Min Li³  Daxiong Zeng⁴  Huihui Jiang⁵  Ke Zhu⁵  Ran Wang⁵  Li Sun⁵  Binbin Zhang⁵  Sijing Zhou⁶ 

[1] Corresponding author: Daxiong Zeng, PhD, Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou 215006, China.;Department of General Medicine, Hefei Second People’s Hospital, Hefei 230001, China;Department of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China;Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou 215006, China;Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China;Hefei Prevention and Treatment Center for Occupational Diseases, Hefei 230022, China;

关键词: COPD;    microbiota;    miRNA;    IL-17a;    lactobacillus;   

DOI  :  

来源: DOAJ

【 摘 要 】

The changes of microbiota in lungs could change interleukin-17a (IL-17a) expression by altering microRNAs (miRNAs) profile, thus contributing to the pathogenesis of chronic obstructive pulmonary disease (COPD). In this study, we aimed to study molecular mechanisms’ underlying effect of microbiota imbalance on COPD deterioration. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were performed to analyze expression of miRNAs and IL-17a mRNA. ELISA was used to evaluate abundance of IL-17a in plasma, peripheral blood monocyte, and sputum of COPD mice and patients. Luciferase assay was performed to explore underlying molecular mechanisms. The expression of miR-122, miR-30a, and miR-99b were remarkably decreased in COPD mice, while the expression of IL-17a was notably increased in plasma, peripheral blood monocytes, and lung tissues of COPD mice. The levels of Lactobacillus/Moraxella and IL-17a expression were significantly enhanced in sputum of exacerbated COPD patients, along with notably decreased expression of miR-122 and miR-30a. Luciferase assay confirmed that miR-122 and miR-30a played an inhibitory role in IL-17a expression. We identified miR-122 and miR-30a as differentially expressed miRNAs in sputum and plasma of COPD patients in exacerbation-month12 group. Furthermore, downregulated miR-122 and miR-30a expression associated with microbiota imbalance may contribute to COPD deterioration by enhancing IL-17a production.

【 授权许可】

Unknown