Xiao-qing-long-tang ameliorates OVA-induced allergic rhinitis by inhibiting ILC2s through the IL-33/ST2 and JAK/STAT pathways.
Animals
Mice
Ovalbumin
Immunity, Innate
Interleukin-1 Receptor-Like 1 Protein
/ metabolism
Janus Kinases
/ metabolism
Interleukin-33
/ metabolism
Lymphocytes
Signal Transduction
STAT Transcription Factors
/ metabolism
Rhinitis, Allergic
/ chemically induced
Cytokines
/ metabolism
Disease Models, Animal
Mice, Inbred BALB C
Allergic rhinitis
IL-33/ST2 signaling
ILC2s
JAK/STAT pathway
Xiao-qing-long-tang
Journal
Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794
Informations de publication
Date de publication:
Oct 2023
Oct 2023
Historique:
received:
18
10
2022
revised:
27
07
2023
accepted:
02
08
2023
medline:
31
8
2023
pubmed:
17
8
2023
entrez:
16
8
2023
Statut:
ppublish
Résumé
Allergic rhinitis (AR) is a chronic inflammatory disease of the nasal mucosa that is mediated by immunoglobulin E (IgE). Xiao-qing-long-tang (XQLT) is a traditional Chinese medicine compound that is widely used to treat respiratory diseases such as AR. However, the underlying mechanism of the effect of XQLT on AR remains unclear. To elucidate the effect of XQLT on ovalbumin (OVA)-induced AR and the mechanisms of action. The therapeutic efficacy of XQLT was evaluated in a well-established OVA-induced AR mouse model. Nasal symptoms were analyzed, type 2 cytokines and OVA-sIgE levels were measured, nasal mucosa tissues were collected for histological analysis, and the changes of Group 2 innate lymphoid cells (ILC2s) and the IL-33/ST2 and JAK/STAT signaling pathways in the nasal mucosa were observed. XQLT significantly alleviated the nasal symptoms and histological damage to the nasal mucosa in AR mice, and reduced the levels of type 2 cytokines and OVA-sIgE. In addition, after XQLT treatment, the numbers of ILC2s in the nasal mucosa of AR mice were reduced, and the mRNA levels of the transcription factors GATA3 and ROR-α were decreased. Moreover, IL-33/ST2 signaling pathway was inhibited. The costimulatory cytokine associated JAK/STAT signaling pathway was also inhibited in ILC2s. Our study demonstrated that XQLT regulated ILC2s through the IL-33/ST2 and JAK/STAT pathways to ameliorate type 2 inflammation in OVA-induced AR. These findings suggest that XQLT might be used to treat AR.
Sections du résumé
BACKGROUND
BACKGROUND
Allergic rhinitis (AR) is a chronic inflammatory disease of the nasal mucosa that is mediated by immunoglobulin E (IgE). Xiao-qing-long-tang (XQLT) is a traditional Chinese medicine compound that is widely used to treat respiratory diseases such as AR. However, the underlying mechanism of the effect of XQLT on AR remains unclear.
PURPOSE
OBJECTIVE
To elucidate the effect of XQLT on ovalbumin (OVA)-induced AR and the mechanisms of action.
METHODS
METHODS
The therapeutic efficacy of XQLT was evaluated in a well-established OVA-induced AR mouse model. Nasal symptoms were analyzed, type 2 cytokines and OVA-sIgE levels were measured, nasal mucosa tissues were collected for histological analysis, and the changes of Group 2 innate lymphoid cells (ILC2s) and the IL-33/ST2 and JAK/STAT signaling pathways in the nasal mucosa were observed.
RESULTS
RESULTS
XQLT significantly alleviated the nasal symptoms and histological damage to the nasal mucosa in AR mice, and reduced the levels of type 2 cytokines and OVA-sIgE. In addition, after XQLT treatment, the numbers of ILC2s in the nasal mucosa of AR mice were reduced, and the mRNA levels of the transcription factors GATA3 and ROR-α were decreased. Moreover, IL-33/ST2 signaling pathway was inhibited. The costimulatory cytokine associated JAK/STAT signaling pathway was also inhibited in ILC2s.
CONCLUSION
CONCLUSIONS
Our study demonstrated that XQLT regulated ILC2s through the IL-33/ST2 and JAK/STAT pathways to ameliorate type 2 inflammation in OVA-induced AR. These findings suggest that XQLT might be used to treat AR.
Identifiants
pubmed: 37586158
pii: S0944-7113(23)00373-2
doi: 10.1016/j.phymed.2023.155012
pii:
doi:
Substances chimiques
Ovalbumin
9006-59-1
sho-seiryu-to
0
Interleukin-1 Receptor-Like 1 Protein
0
Janus Kinases
EC 2.7.10.2
Interleukin-33
0
STAT Transcription Factors
0
Cytokines
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
155012Informations de copyright
Copyright © 2023. Published by Elsevier GmbH.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.