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Int. J. Mol. Sci. 2018, 19(8), 2456; https://doi.org/10.3390/ijms19082456

Toll-Like Receptor Agonists Modulate Wound Regeneration in Airway Epithelial Cells

1
Department of Rheumatology, Chair of Clinical Immunology and Rheumatology, Medical University of Lodz, 90-419 Lodz, Poland
2
Department of Microbiology and Medical Laboratory Immunology, Medical University of Lodz, 90-419 Lodz, Poland
3
Department of Immunology and Allergy, Chair of Clinical Immunology and Rheumatology, Medical University of Lodz, 90-419 Lodz, Poland
*
Author to whom correspondence should be addressed.
Received: 10 July 2018 / Revised: 7 August 2018 / Accepted: 16 August 2018 / Published: 20 August 2018
(This article belongs to the Special Issue New Innovations in Wound Healing and Repair)
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Abstract

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. View Full-Text
Keywords: airway epithelium; wound repair; TLRs; poly(I:C); LPS airway epithelium; wound repair; TLRs; poly(I:C); LPS
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Lewandowska-Polak, A.; Brauncajs, M.; Jarzębska, M.; Pawełczyk, M.; Kurowski, M.; Chałubiński, M.; Makowska, J.; Kowalski, M.L. Toll-Like Receptor Agonists Modulate Wound Regeneration in Airway Epithelial Cells. Int. J. Mol. Sci. 2018, 19, 2456.

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