STAT1 participates in the induction of substance P expression in airway epithelial cells by respiratory syncytial virus.
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| Abstract | PURPOSE: The regulation effect and mechanism of respiratory syncytial virus (RSV) infection on the expression of tachykinin substance P (SP) in airway epithelial cells was investigated. METHODS: The regulation of SP expression by RSV was investigated in the BEAS-2B airway epithelial cell line. RT-qPCR, immunofluorescence, and ELISA assay were used to examine the expression of the SP encoding gene TAC1, the intracellular SP protein expression, and the extracellular SP secretion. RESULTS: The mRNA expression of TAC1 and the intracellular SP protein level in BEAS-2B cells were significantly enhanced by RSV infection with multiplicity of infection (MOI) values of both 1 and 0.1 at 48 hours post infection. Heat-inactivated and UV-inactivated RSV, but not live RSV, significantly induced SP secretion in both control BEAS-2B cells and CX3CR1 receptor knockout cells without affecting the TAC1 gene expression or cell viability. RSV G protein (2-10 μg/ml) and fractalkine (10-50 ng/ml), both CX3CR1 receptor ligands, did not affect SP secretion in BEAS-2B cells. Inhibition of STAT1 phosphorylation by fludarabine (1 μM) markedly reduced the RSV-induced TAC1 gene expression and antagonized the inhibition of RSV replication by interferon-α in BEAS-2B cells. CONCLUSIONS: STAT1 participates in RSV infection-induced SP expression in airway epithelial cells.
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| Authors | Yu-Long Luo, Sheng Wang, Zhi-Xin Fang, Yi-Chu Nie, Li-Ting Zhang, Chu-Qin Huang, Li Long, Ke-Fang Lai |
| Journal | Experimental lung research (Exp Lung Res) 2021 Feb-Mar Vol. 47 Issue 2 Pg. 78-86 ISSN: 1521-0499 [Electronic] England |
| PMID | 33238771 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
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