Cigarette Smoke Underlies the Pathogenesis of Palmoplantar Pustulosis via an IL-17A-Induced Production of IL-36γ in Tonsillar Epithelial Cells.
Adult
Aged
Cells, Cultured
Cigarette Smoking
/ adverse effects
Epithelial Cells
/ immunology
Ex-Smokers
/ statistics & numerical data
Female
Humans
Interleukin-1
/ metabolism
Interleukin-17
/ metabolism
Male
Middle Aged
Non-Smokers
/ statistics & numerical data
Palatine Tonsil
/ cytology
Primary Cell Culture
Psoriasis
/ diagnosis
Severity of Illness Index
Signal Transduction
/ immunology
Smoke
/ adverse effects
Smokers
/ statistics & numerical data
Nicotiana
/ adverse effects
Journal
The Journal of investigative dermatology
ISSN: 1523-1747
Titre abrégé: J Invest Dermatol
Pays: United States
ID NLM: 0426720
Informations de publication
Date de publication:
06 2021
06 2021
Historique:
received:
07
05
2020
revised:
24
08
2020
accepted:
09
09
2020
pubmed:
15
11
2020
medline:
20
11
2021
entrez:
14
11
2020
Statut:
ppublish
Résumé
Palmoplantar pustulosis (PPP) is characterized by sterile pustules on the palms and soles. A strong association between PPP and tobacco smoking has been reported, and it has been speculated that the IL-17A pathway may play an important role in PPP. Recent studies have suggested that IL-36 plays a pivotal role in the pathogenesis of psoriasis and its subtypes. The relationships among IL-36, smoking, and PPP have not been examined. Here, we investigated the relationships among the smoking index, severity of the clinical condition of PPP, and in vitro dynamics of IL-36 in human tonsillar epithelial cells under the condition of exposure to a cigarette smoke extract. The results demonstrated that the Palmoplantar Pustulosis Area and Severity Index was strongly and positively correlated with the smoking index in female patients. Immunohistochemical examinations showed that IL-36γ was highly expressed in tonsillar epithelial cells from patients with PPP but not in those from patients with recurrent tonsillitis without PPP. The in vitro study revealed that IL-17A synergistically induced a release of IL-36γ under cigarette smoke extract exposure. These results suggest that local production of IL-36γ by epithelial cells induced by cigarette smoke exposure plays an important role in the pathogenesis of PPP.
Identifiants
pubmed: 33188781
pii: S0022-202X(20)32277-6
doi: 10.1016/j.jid.2020.09.028
pii:
doi:
Substances chimiques
IL17A protein, human
0
IL36G protein, human
0
Interleukin-1
0
Interleukin-17
0
Smoke
0
Types de publication
Journal Article
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1533-1541.e4Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.