The relationship between IL-17A and IL-22 expression and clinical severity in patients with moderate/severe persistent allergic rhinitis.
Journal
American journal of otolaryngology
ISSN: 1532-818X
Titre abrégé: Am J Otolaryngol
Pays: United States
ID NLM: 8000029
Informations de publication
Date de publication:
Historique:
received:
12
10
2018
revised:
14
12
2018
accepted:
18
12
2018
pubmed:
31
12
2018
medline:
22
6
2019
entrez:
31
12
2018
Statut:
ppublish
Résumé
Several reactions leading to numerous effects are regulated by IL-22. However, the relationship between IL-22 and immunopathogensis of allergic rhinitis (AR) has been rarely investigated. The aim of the present study was to investigate the levels of IL-22 and IL-17A in AR patients and their association with clinical severity of persistent allergic rhinitis (PAR). Thirty mild persistent allergic rhinitis (M PAR) patients, thirty moderate/severe persistent allergic rhinitis (M/S PAR) patients, and thirty healthy controls were enrolled in this study. Local production of IL-22 and IL-17A in PAR patients and healthy controls' nasal mucosa was examined by immunohistochemistry (IHC) and real-time polymerase chain reaction (RT-PCR) techniques. Serum levels of IL-22, IL-17A, specific immunoglobulin E (sIgE), and total IgE (tIgE) in PAR patients and healthy controls were determined by ELISA. In addition, blood eosinophil, nasal eosinophils per field, and total nasal syndrome score (TNSS) were also assessed. In comparison with healthy controls, production of IL-22 and IL-17A in M/S PAR patients increased significantly. Furthermore, serum levels as well as the mean number of IL-22 The results of the present study provide the first evidence that local production of IL-22 might be expressed in PAR patients. The expression of IL-22 and IL-17A, and their correlations with clinical parameters in PAR patients suggest the role of these cytokines in the events involved in the development of PAR.
Identifiants
pubmed: 30594402
pii: S0196-0709(18)30951-7
doi: 10.1016/j.amjoto.2018.12.009
pii:
doi:
Substances chimiques
Biomarkers
0
IL17A protein, human
0
Inflammation Mediators
0
Interleukin-17
0
Interleukins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
173-178Informations de copyright
Copyright © 2018. Published by Elsevier Inc.