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

International Journal of Molecular Sciences

Maciej Chałubiński¹  MarekL. Kowalski¹  Marzanna Jarzębska¹  Małgorzata Pawełczyk¹  Marcin Kurowski¹  Małgorzata Brauncajs²  Anna Lewandowska-Polak³  Joanna Makowska³ 

[1] Department of Immunology and Allergy, Chair of Clinical Immunology and Rheumatology, Medical University of Lodz, 90-419 Lodz, Poland;Department of Microbiology and Medical Laboratory Immunology, Medical University of Lodz, 90-419 Lodz, Poland;Department of Rheumatology, Chair of Clinical Immunology and Rheumatology, Medical University of Lodz, 90-419 Lodz, Poland;

关键词: airway epithelium;    wound repair;    TLRs;    poly(I:C);    LPS;   

DOI  :  10.3390/ijms19082456

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown