- Title
- Effect of human rhinovirus infection on airway epithelium tight junction protein disassembly and transepithelial permeability
- Creator
- Looi, Kevin; Troy, Niamh M.; Sutanto, Erika N.; Zosky, Graeme R.; Rigby, Paul J.; Larcombe, Alexander N.; Knight, Darryl A.; Kicic, Anthony; Stick, Stephen M.; Garratt, Luke W.; Iosifidis, Thomas; Bosco, Anthony; Buckley, Alysia G.; Ling, Kak-Ming; Martinovich, Kelly M.; Kicic-Starcevich, Elizabeth; Shaw, Nicole C.
- Relation
- NHMRC.1026494
- Relation
- Experimental Lung Research Vol. 42, Issue 7, p. 380-395
- Publisher Link
- http://dx.doi.org/10.1080/01902148.2016.1235237
- Publisher
- Taylor & Francis
- Resource Type
- journal article
- Date
- 2016
- Description
- Rationale: No studies have assessed the effects of human rhinovirus (HRV) infection on epithelial tight junctions (TJs) and resultant barrier function. Aim of the Study: To correlate viral infection with TJ disassembly, epithelial barrier integrity, and function. Materials and Methods: Human airway epithelial cells were infected with HRV minor serotype 1B (HRV-1B) at various 50% tissue culture infectivity doses (TCID⁵⁰) 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-CellTM Western assays. Transepithelial permeability assays were performed to assess effects on barrier functionality. RT2 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. Results: HRV-1B infection affected viability that was both time and TCID⁵⁰ 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 TCID⁵⁰, while a significant decrease in all three TJ protein expressions occurred at higher TCID⁵⁰. 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. Conclusion: HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via an antiviral response of IL-15.
- Subject
- HRV replication; epithelial cells; tissue culture; viral infection
- Identifier
- http://hdl.handle.net/1959.13/1329212
- Identifier
- uon:26099
- Identifier
- ISSN:0190-2148
- Language
- eng
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