Staphylococcus aureus impairs the airway epithelial barrier in vitro

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dc.contributor.authorMalik, Z.
dc.contributor.authorRoscioli, E.
dc.contributor.authorMurphy, J.
dc.contributor.authorOu, J.
dc.contributor.authorBassiouni, A.
dc.contributor.authorWormald, P.
dc.contributor.authorVreugde, S.
dc.date.issued2015
dc.descriptionPublished online: 26 MAR 2015
dc.description.abstractBackground: Chronic rhinosinusitis (CRS) is a cluster of disorders that result in sinonasal mucosal inflammation. Staphylococcus aureus (S. aureus) is associated with severe and recalcitrant CRS. The purpose of our study was to investigate the effect of S. aureus on respiratory epithelial barrier structure and function. Methods: Conditioned media from S. aureus reference strains (American Type Culture Collection [ATCC] 13565, 14458, and 25923) was applied to air-liquid interface (ALI) cultures of primary human nasal epithelial cells (HNECs) and transepithelial electrical resistance (TEER) was measured to assess cell-to-cell integrity. Electron microscopy was used to gauge the ciliated area and tight junctions (TJs). Additionally, the expression of the TJ protein zona occludens-1 (ZO-1) was examined via immunofluorescence. Statistical analysis was performed using analysis of variance (ANOVA) with pairwise Bonferroni-adjusted t tests. Results: Secreted products applied to ALI cultures from S. aureus strain 13565 caused a concentration-dependent decline in electrical impedance compared to controls and reference strains 14458 and 25923 (p < 0.001). Electron microscopy showed a distinct separation between adjacent cells apically, in the region of TJs. The ciliated area was not affected; however, ZO-1 expression became discontinuous in HNECs exposed to the 13565 strain's conditioned media. Conclusion: Conditioned media of the S. aureus strain 13565 damages the airway epithelium by disrupting the TJs between primary HNECs grown at an ALI. These findings suggest that strain-specific S. aureus-secreted product(s) compromise epithelial barrier function, which may constitute 1 of the roles played by S. aureus in the pathophysiology of recalcitrant CRS. Further research is required to uncover the relevant molecular mechanisms.
dc.description.statementofresponsibilityZacki Malik, Eugene Roscioli, Jae Murphy, Judy Ou, Ahmed Bassiouni, Peter-John Wormald, and Sarah Vreugde
dc.identifier.citationInternational Forum of Allergy and Rhinology, 2015; 5(6):551-556
dc.identifier.doi10.1002/alr.21517
dc.identifier.issn2042-6976
dc.identifier.issn2042-6984
dc.identifier.orcidRoscioli, E. [0000-0002-3201-3899]
dc.identifier.orcidBassiouni, A. [0000-0002-5545-0194]
dc.identifier.orcidWormald, P. [0000-0001-7753-7277]
dc.identifier.orcidVreugde, S. [0000-0003-4719-9785]
dc.identifier.urihttp://hdl.handle.net/2440/92585
dc.language.isoen
dc.publisherWiley
dc.rights© 2015 ARS-AAOA, LLC
dc.source.urihttps://doi.org/10.1002/alr.21517
dc.subjectAir-liquid interface; chronic rhinosinusitis; epithelium; electric impedance; tight junctions
dc.titleStaphylococcus aureus impairs the airway epithelial barrier in vitro
dc.typeJournal article
pubs.publication-statusPublished

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