β-defensin-1 regulates influenza virus infection in human bronchial epithelial cells through the STAT3 signaling Pathway

نویسندگان

چکیده

Abstract To develop intervention strategies it is necessary to understand the host response influenza A virus (IAV) infection. The primary barriers for invading respiratory pathogens are airway epithelial cells of tract and several antimicrobial peptides produced by these cells. peptide, β-defensin-1, has antiviral activity against both enveloped non-enveloped viruses. Significant downregulation β-defensin-1 gene (DEFB1) expression was observed when human bronchial (HBEpCs) were exposed IAV. HBEpCs overexpressing DEFB1caused a significant reduction in IAV, that confirmed IAV matrix analysis, plaque assay, confocal microscopy. DEFB1expression after transfection with two micro RNAs (miRNAs), hsa-miR-186-5p hsa-miR-340-5p, provided evidence could be modulated miRNAs had higher binding efficiency DEFB1. Overexpression DEFB1in infected led increased NF-κB expression. In PCR array analysis 84 transcription factors, either DEFB1or siRNA silencing significantly signal transducer activator 3 (STAT3). addition, Ingenuity Pathway Analysis (IPA) integrated data showed JAK1/STAT3 pathway altered DEFB1, suggesting this one pathways which defensin regulates replication HBEpCs. conclusion, copy number DEFB1overexpressing suggests plays key role regulating survival through STAT3 potential target drug development. No funding

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ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2023

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.210.supp.235.01