The LncRNA Malat1 Moduate The Maturation Process,Pro-inflammatory Cytokine Secretion,apoptosis In Airway Epithelial Cells Conditioned Dendritic Cell

Background and Objective:Airway epithelial cells(AECs)are the first point of contact with airborne antigens and are able to instruct resident imlune cells to appropriate immune responses.Amounting evidence indicated that abnormal expression of Malatl participated in various cell types.The aim of this study was to identify the Malatl as a new epithelial cell-derived immune-modulating factors that contribute to the definition of a specific inflammatory-immune airway microenvironment.Methods:Airway epithelial cells were cultured with Malatl siRNA,then using an in-vitro co-culture model of the airway epithelium,where cell layer of Airway epithelial cells can interact with dendritic cells(DCs).The DC immunophenotype and Annexin-V were analyzed by flow cytometric,supernatants were collected to determine inflammatory chemokine markers,Results:The results revealed a significant diminution of Malatl expression after Malatl siRNA treated,Meanwhile,we confirm that Malatl partly induces the maturation of DCs that were cultured in AEC-conditioned medium.The mRNA and protein levels of some siarface molecules(i.e.,CD80,CD86 and MHC?)of AEC-conditioned treated DCs were upregulated in response to incubation with Malatl inhibitor.Meanwhile Malatl inhibitor increased the inflarmatory cytokines TNF-a,IL-65INF-r secretion significantly(more than 3-5 fold in RNA level and about 2 fold in protein level)and the level of IL-4 was downregulated by Malatl inhibitor slightly(50%off).The mean apoptotic cell fractions(early apoptotic+late apoptotic)were significantly decreased upon Malatl inhibition compared with the control,with a concomitant increase in the viable cell populationConclusion:Our study clearly revealed that the IncRNA Malatl modulate the maturation process,pro-inflammatory cytokine secretion and apoptosis in airway epithelial cells conditioned dendritlc cell.