Effect of human rhinovirus infection on airway epithelium tight junction protein disassembly and transepithelial permeability
MetadataShow full item record
© 2016 Taylor & Francis. 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 (TCID 50 ) 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-Cell™ Western assays. Transepithelial permeability assays were performed to assess effects on barrier functionality. RT 2 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 TCID 50 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 50 , while a significant decrease in all three TJ protein expressions occurred at higher TCID 50 . 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.
Showing items related by title, author, creator and subject.
Modelling the co-occurence of Streptococcus pneumoniae with other bacterial and viral pathogens in the upper respiratory tractJacoby, P.; Watson, K.; Bowman, J.; Taylor, A.; Riley, T.; Smith, D.; Lehmann, Deborah (2007)Go to ScienceDirect® Home Skip Main Navigation Links Brought to you by: The University of Western Australia Library Login: + Register Athens/Institution Login Not Registered? - User Name: Password: ...
Looi, K.; Buckley, A.; Rigby, P.; Garratt, L.; Iosifidis, T.; Zosky, G.; Larcombe, Alexander; Lannigan, F.; Ling, K.; Martinovich, K.; Kicic-Starcevich, E.; Shaw, N.; Sutanto, E.; Knight, D.; Kicic, A.; Stick, S. (2018)© 2018 John Wiley & Sons Ltd Background: Bronchial epithelial tight junctions (TJ) have been extensively assessed in healthy airway epithelium. However, no studies have yet assessed the effect of human rhinovirus (HRV) ...
Therapeutic impact of human serum albumin-thioredoxin fusion protein on influenza virus-induced lung injury miceTanaka, R.; Ishima, Y.; Enoki, Y.; Kimachi, K.; Shirai, T.; Watanabe, H.; Chuang, Victor; Maruyama, T.; Otagiri, M. (2014)Reactive oxygen species (ROS) are the primary pathogenic molecules produced in viral lung infections. We previously reported on the use of a recombinant human serum albumin (HSA)-thioredoxin 1 (Trx) fusion protein (HSA-Trx) ...