Toll-Like Receptor Agonists Modulate Wound Regeneration in Airway Epithelial Cells.
Int J Mol Sci
; 19(8)2018 Aug 20.
Article
em En
| MEDLINE
| ID: mdl-30127243
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(IC), 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(IC) 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(IC)-induced repair inhibition. TGF-ß and RANTES mRNA expression was higher in injured ECs and IFN-α, IFN-ß, IL-8, and VEGF mRNA expression was lower in damaged epithelium as compared to not-injured. Stimulation with poly(IC) increased IFN-α and IFN-ß 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.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Regeneração
/
Cicatrização
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Mucosa Respiratória
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Receptores Toll-Like
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
Polônia