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Published on: June 13, 2019
Toll-Like Receptor Agonists Modulate Wound Regeneration in Airway Epithelial Cells
Anna Lewandowska-Polak1, Małgorzata Brauncajs2, Marzanna Jarzębska3
1Department of Rheumatology, Chair of Clinical Immunology and Rheumatology, Medical University of Lodz, 90-419 Lodz, Poland. anna.lewandowska-polak@umed.lodz.pl.
Background:
Impaired regeneration of airway epithelium may lead to persistence of inflammation and remodelling. Regeneration of injured epithelium is a complex phenomenon and the role of toll-like receptors (TLRs) in the stimulation of respiratory virus products in this process has not been established.
Objective:
This study was undertaken to test the hypothesis that the wound repair process in airway epithelium is modulated by microbial products via toll-like receptors.
Methods:
Injured and not-injured bronchial epithelial cells (ECs) (BEAS-2B line) were incubated with the TLR agonists poly(I:C), lipopolisacharide (LPS), allergen Der p1, and supernatants from virus-infected epithelial cells, either alone or in combination with TLR inhibitors. Regeneration and immune response in injured and not-injured cells were studied.
Results:
Addition of either poly(I:C) or LPS to ECs induced a marked inhibition of wound repair. Supernatants from RV1b-infected cells also decreased regeneration. Preincubation of injured and not-injured ECs with TLR inhibitors decreased LPS and poly(I:C)-induced repair inhibition. TGF-β and RANTES mRNA expression was higher in injured ECs and IFN-α, IFN-β, IL-8, and VEGF mRNA expression was lower in damaged epithelium as compared to not-injured. Stimulation with poly(I:C) increased IFN-α and IFN-β mRNA expression in injured cells, and LPS stimulation decreased interferons mRNA expression both in not-injured and injured ECs.
Conclusion:
Regeneration of the airway epithelium is modulated by microbial products via toll-like receptors.
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