Location of eosinophils in the airway wall is critical for specific features of airway hyperresponsiveness and T2 inflammation in asthma.
Journal
The European respiratory journal
ISSN: 1399-3003
Titre abrégé: Eur Respir J
Pays: England
ID NLM: 8803460
Informations de publication
Date de publication:
08 2022
08 2022
Historique:
received:
02
07
2021
accepted:
06
12
2021
pubmed:
15
1
2022
medline:
9
8
2022
entrez:
14
1
2022
Statut:
epublish
Résumé
Eosinophils are implicated as effector cells in asthma, but the functional implications of the precise location of eosinophils in the airway wall is poorly understood. We aimed to quantify eosinophils in the different compartments of the airway wall and associate these findings with clinical features of asthma and markers of airway inflammation. In this cross-sectional study, we utilised design-based stereology to accurately partition the numerical density of eosinophils in both the epithelial compartment and the subepithelial space (airway wall area below the basal lamina including the submucosa) in individuals with and without asthma and related these findings to airway hyperresponsiveness (AHR) and features of airway inflammation. Intraepithelial eosinophils were linked to the presence of asthma and endogenous AHR, the type that is most specific for asthma. In contrast, both intraepithelial and subepithelial eosinophils were associated with type 2 (T2) inflammation, with the strongest association between We conclude that intraepithelial eosinophils are associated with endogenous AHR and T2 inflammation and may interact with intraepithelial mast cells
Sections du résumé
BACKGROUND
Eosinophils are implicated as effector cells in asthma, but the functional implications of the precise location of eosinophils in the airway wall is poorly understood. We aimed to quantify eosinophils in the different compartments of the airway wall and associate these findings with clinical features of asthma and markers of airway inflammation.
METHODS
In this cross-sectional study, we utilised design-based stereology to accurately partition the numerical density of eosinophils in both the epithelial compartment and the subepithelial space (airway wall area below the basal lamina including the submucosa) in individuals with and without asthma and related these findings to airway hyperresponsiveness (AHR) and features of airway inflammation.
RESULTS
Intraepithelial eosinophils were linked to the presence of asthma and endogenous AHR, the type that is most specific for asthma. In contrast, both intraepithelial and subepithelial eosinophils were associated with type 2 (T2) inflammation, with the strongest association between
CONCLUSIONS
We conclude that intraepithelial eosinophils are associated with endogenous AHR and T2 inflammation and may interact with intraepithelial mast cells
Identifiants
pubmed: 35027395
pii: 13993003.01865-2021
doi: 10.1183/13993003.01865-2021
pmc: PMC9704864
mid: NIHMS1852157
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIAID NIH HHS
ID : K24 AI130263
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI130280
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI163160
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI125378
Pays : United States
Organisme : NIAID NIH HHS
ID : K24 AI150991
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL153979
Pays : United States
Informations de copyright
Copyright ©The authors 2022. For reproduction rights and permissions contact permissions@ersnet.org.
Déclaration de conflit d'intérêts
Conflict of interest: T. Al-Shaikhly has a patent MicroRNAs as Predictors of Response to Anti-IgE Therapies in Chronic Spontaneous Urticaria pending. M.C. Altman reports personal fees from Sanofi-Regeneron outside the submitted work. W.A. Altemeier reports grants from the National Institute of Health during the conduct of the study. J.S. Debley reports grants from the National Institute of Health during the conduct of the study. A.M. Piliponsky reports grants from the National Institute of Health outside the submitted work. M.C. Peters reports grants from National Institute of Health-NHLBI, Boehringer Ingelheim, AstraZeneca, Boehringer Ingelheim, Genentech, GlaxoSmithKline, Sanofi-Genzyme-Regeneron and Teva, outside the submitted work. T.S. Hallstrand reports grants from the National Institute of Health during the conduct of the study. The remaining authors report no competing financial interests.
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