English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Infection plays a significant role in the relapse of chronic rhinosinusitis (CRS), however, the role of primary human nasal epithelial cells (HNECs) in this process is largely unknown. Here, we determined the effect of Toll-like receptor (TLR) agonists and inflammatory cytokines on mucosal barrier integrity and immune response of HNECs. TLR 1–9 agonists and inflammatory cytokines were applied to submerged and/or air-liquid interface (ALI) cultures of HNECs from CRS patients and controls for 24 hours. Interleukin-6 (IL-6) protein levels were determined by ELISA. Mucosal barrier integrity was measured via Transepithelial Electrical Resistance and passage of fluorescently-labelled dextrans. IL-1β and IFN- γ significantly increased IL-6 production in HNECs derived from CRS patients and controls, however, a dose-dependent effect was observed in CRS-derived HNECs only. Stimulation with Poly (I:C) LMW induced a 15 to 17 fold increase in IL-6 production by HNEC-ALI control cells (p < 0.05) and HNEC-ALI-CRS cells (p = 0.004) whilst a 2.5 fold increase was observed in CRS HNEC submerged cultures. Priming of cells with Poly (I:C) LMW reduced subsequent IL-6 secretion upon stimulation with TLR 2–4 agonists. Poly (I:C) LMW exerts a potent pro-inflammatory effect on HNECs and reduces a subsequent immune activation by TLR agonists.

Primary human nasal epithelial cells: a source of poly (I:C) LMW-induced IL-6 production