AUTHOR=Hu Qingchang, Zhao Yabo, Wang Zaiwei, Hou Yue, Bi Dingren, Sun Jianjun, Peng Xiuli TITLE=Chicken gga-miR-19a Targets ZMYND11 and Plays an Important Role in Host Defense against Mycoplasma gallisepticum (HS Strain) Infection JOURNAL=Frontiers in Cellular and Infection Microbiology VOLUME=6 YEAR=2016 URL=https://www.frontiersin.org/articles/10.3389/fcimb.2016.00102 DOI=10.3389/fcimb.2016.00102 ISSN=2235-2988 ABSTRACT=Mycoplasma gallisepticum (MG), one of the most pathogenic Mycoplasmas, can cause chronic respiratory disease (CRD) in chickens. It has been suggested that micro-ribonucleic acids (miRNAs) are involved in microbial pathogenesis. However, little is known about the roles of miRNAs in MG infection. Previously, we found by deep sequencing that gga-miR-19a was significantly up-regulated in the lungs of MG-infected chicken embryos. In this work, we confirmed that gga-miR-19a was up-regulated in both MG-infected chicken embryonic lungs and MG-infected DF-1 (chicken embryo fibroblast) cells. At 72 h post-transfection, we found that the over-expression of gga-miR-19a significantly enhanced the proliferation of MG-infected DF-1 cells by promoting the transition from the G1 phase to the S and G2 phases, while a gga-miR-19a inhibitor repressed the proliferation of MG-infected DF-1 cells by arresting the cell cycle in the G1 phase. Moreover, we found that gga-miR-19a regulated the expression of the host zinc-finger protein, MYND-type containing 11 (ZMYND11), through binding to its 3′ untranslated region (3′-UTR). DAVID analysis revealed that ZMYND11 could negatively regulate the NF-kappaB (NF-κB) signaling pathway in chickens (Gallus gallus). Upon MG infection, gga-miR-19a, NF-κB, MyD88, and TNF-α were all up-regulated, whereas ZMYND11 was down-regulated. The over-expression of gga-miR-19a in the DF-1 cells did not affect the above gene expression patterns, and gga-miR-19a inhibitor repressed the expression of NF-κB, MyD88, and TNF-α, but enhanced the expression of ZMYND11. In conclusion, gga-miR-19a might suppress the expression of ZMYND11 in MG-infected chicken embryonic lungs and DF-1 cells, activate the NF-κB signaling pathway, and promote pro-inflammatory cytokines expression, the cell cycle progression and cell proliferation to defend against MG infection.