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Effect of human rhinovirus infection on airway epithelium tight junction protein disassembly and transepithelial permeability.
- Source :
-
Experimental lung research [Exp Lung Res] 2016; Vol. 42 (7), pp. 380-395. Date of Electronic Publication: 2016 Oct 11. - Publication Year :
- 2016
-
Abstract
- Rationale: No studies have assessed the effects of human rhinovirus (HRV) infection on epithelial tight junctions (TJs) and resultant barrier function.<br />Aim of the Study: To correlate viral infection with TJ disassembly, epithelial barrier integrity, and function.<br />Materials and Methods: Human airway epithelial cells were infected with HRV minor serotype 1B (HRV-1B) at various 50% tissue culture infectivity doses (TCID <subscript>50</subscript> ) over 72 hours. HRV replication was assessed by quantitative-polymerase chain reaction (qPCR) while cell viability and apoptosis were assessed by proliferation and apoptotic assays, respectively. Protein expression of claudin-1, occludin, and zonula occludens protein-1 (ZO-1) was assessed using In-Cellâ„¢ Western assays. Transepithelial permeability assays were performed to assess effects on barrier functionality. RT <superscript>2</superscript> Profiler focused qPCR arrays and pathway analysis evaluating associations between human TJ and antiviral response were performed to identify potential interactions and pathways between genes of interests.<br />Results: HRV-1B infection affected viability that was both time and TCID <subscript>50</subscript> dependent. Significant increases in apoptosis and viral replication post-infection correlated with viral titer. Viral infection significantly decreased claudin-1 protein expression at the lower TCID <subscript>50</subscript> , while a significant decrease in all three TJ protein expressions occurred at higher TCID <subscript>50</subscript> . Decrease in protein expression was concomitant with significant increases in epithelial permeability of fluorescein isothiocynate labeled-dextran 4 and 20 kDa. Analysis of focused qPCR arrays demonstrated a significant decrease in ZO-1 gene expression. Furthermore, network analysis between human TJ and antiviral response genes revealed possible interactions and regulation of TJ genes via interleukin (IL)-15 in response to HRV-1B infection.<br />Conclusion: HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via an antiviral response of IL-15.
Details
- Language :
- English
- ISSN :
- 1521-0499
- Volume :
- 42
- Issue :
- 7
- Database :
- MEDLINE
- Journal :
- Experimental lung research
- Publication Type :
- Academic Journal
- Accession number :
- 27726456
- Full Text :
- https://doi.org/10.1080/01902148.2016.1235237