The mechanism on Prevotella melaninogenica promoting the inflammatory progression of oral lichen planus.
Prevotella melaninogenica
IL-36γ
oral lichen planus
Journal
Clinical and experimental immunology
ISSN: 1365-2249
Titre abrégé: Clin Exp Immunol
Pays: England
ID NLM: 0057202
Informations de publication
Date de publication:
19 08 2022
19 08 2022
Historique:
received:
19
01
2022
revised:
25
04
2022
accepted:
21
05
2022
pubmed:
24
5
2022
medline:
24
8
2022
entrez:
23
5
2022
Statut:
ppublish
Résumé
Oral lichen planus (OLP) is a common chronic inflammatory disease occurring in the oral mucosa. Bacteria are a key driver of mucosal immune responses and can induce changes in gene expression and function of epithelial keratinocytes. IL-36γ can induce the expression of antimicrobial peptides, cytokines, and chemokines, and is widely involved in many chronic inflammatory diseases. Our aim is to explore the role of IL-36γ in the pathological process of OLP when Prevotella melaninogenica (P. melaninogenica) invades the oral mucosa. The expression of IL-36γ in OLP lesions and mice was detected by immunohistochemistry. Recombinant human IL-36Gamma (rhIL-36γ) was used to treat oral keratinocytes and the expression levels of inflammatory cytokines were detected by qRT-PCR and ELISA. The expression of IL-36γ and TRPV1 was detected by western blotting following co-culturing P. melaninogenica with oral keratinocytes. The mRNA expression of IL-36γ was detected by qRT-PCR. From our results, IL-36γ was upregulated in OLP lesions. Exogenous rhIL-36γ promoted the expression of pro-inflammatory cytokines and antibacterial peptides in oral keratinocytes. The expression of IL-36γ was significantly increased following the stimulation of P. melaninogenica in oral keratinocytes and mice. TRPV1 activation was induced by P. melaninogenica and its activation enhanced the expression of IL-36γ. IL-36Ra could reduce the inflammation in OLP in vitro. In summary, overexpression of IL-36γ in OLP lesions could promote its pathogenesis by inducing inflammation. P. melaninogenica invasion of oral keratinocytes could induce the expression of IL-36γ by the activation of TRPV1, thereby regulating the interaction between bacteria and oral epithelial cells.
Identifiants
pubmed: 35605143
pii: 6590871
doi: 10.1093/cei/uxac054
pmc: PMC9390840
doi:
Substances chimiques
Cytokines
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
215-224Informations de copyright
© The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Immunology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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