The modulation of MiR-155 and MiR-23a manipulates Klebsiella pneumoniae Adhesion on Human pulmonary Epithelial cells via Integrin α5β1 Signaling

• Published in: Scientific reports Vol. 6; no. 1; p. 31918
• Main Authors: Teng, Yan, Miao, Junming, Shen, Xiaofei, Yang, Xiaolong, Wang, Xinyuan, Ren, Laibin, Wang, Xiaoying, Chen, Junli, Li, Jingyu, Chen, Shanze, Wang, Yi, Huang, Ning
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 18.08.2016; Nature Publishing Group
• Subjects: 13/89; 14/34; 14/63; 38/1; 38/15; 631/250/2499; 631/250/254; Humanities and Social Sciences; multidisciplinary; Science
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/srep31918

Micro-RNAs (miRNAs) critically regulate several host defense mechanisms, but their roles in the bacteria-epithelium interplay remain unclear. Our results displayed that the expression of miR-155 and miR-23a were down-regulated in K . pneumoniae -infected pulmonary epithelial cells. The elevated bacterial adhesion on A549 cells followed the enhancement of the cellular levels of these two miRNAs. Meanwhile, a mechanistic study demonstrated that miR-155 promoted integrin α5β1 function and resulted in the increased actin polymerization. Moreover, a non-histone nuclear protein, high mobility group nucleosomal-binding domain 2 (HMGN2) served as the potential target of miR-155 and miR-23a to regulate the integrin α5β1 expression and K . pneumoniae adhesion. Furthermore, the expression of a known integrin transcription suppressor-Nuclear Factor-I (NFI) was also repressed by miR-155, which paralleled with its chromatin location in the promoter regions of integrin α5 and β1. These results uncover novel links between miRNAs and integrin function to regulate bacterial adhesion, indicating a potential mechanism of host cell autonomous immune response to K . pneumoniae infection.