Estrogen stimulates Th2 cytokine production and regulates the compartmentalisation of eosinophils during allergen challenge in a mouse model of asthma

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dc.contributor.authorCai, Yeping
dc.contributor.authorZhou, Jiansheng
dc.contributor.authorWebb, Dianne
dc.date.accessioned2015-12-10T23:16:02Z
dc.date.issued2012
dc.date.updated2016-02-24T08:35:05Z
dc.description.abstractBackground: The observation that asthma becomes more prevalent following puberty in females suggests estrogen potentiates the development of this disease. However, most studies examining the role of estrogen in rodent models of asthma are complicated by their reliance on ovariectomised mice in which hormones other than estrogen are also attenuated. Methods: We aimed to understand the influence of estrogen on allergic airway disease by using type I (tamoxifen) or type II (ICI 182,780) antagonists in female mice or delivering estradiol to male mice during aeroallergen challenge. Results: The antagonists showed that estrogen promoted both the mobilisation of bone marrow eosinophils and egression of eosinophils to the airway lumen. These findings were corroborated in male mice treated with estradiol, which increased eosinophil numbers in both blood and airways. Estrogen stimulated goblet cell hyperplasia and baseline lung resistance, but had little effect on the number of eosinophils in the bronchial submucosa or methacholine-induced airway hyperreactivity. Estrogen receptor α was expressed by CD4+ T cells from allergic mice, and estrogen promoted the production of IL-5 and IL-13, and suppressed the production of the eicosanoid 12-HETE by mediastinal lymph node cells. Conclusions: These data show that during aeroallergen challenge, estrogen stimulates Th2 cytokine production, which may be linked to its ability to suppress 12-HETE. Lung resistance at baseline, goblet cell hyperplasia and the compartmentalisation of eosinophils was also influenced by estrogen. However, estrogen does not play a major role in stimulating enhanced sensitivity to methacholine-induced lung resistance.
dc.identifier.issn1018-2438
dc.identifier.urihttp://hdl.handle.net/1885/64895
dc.publisherS Karger AG
dc.sourceInternational Archives of Allergy and Immunology
dc.subjectKeywords: 12 hydroxyicosatetraenoic acid; allergen; estradiol; estrogen; estrogen receptor alpha; fulvestrant; interleukin 13; interleukin 5; methacholine; tamoxifen; animal cell; animal experiment; animal model; animal tissue; article; asthma; blood; bone marrow; Asthma; Eosinophils; Estrogen; IL-13; IL-5; Mucus
dc.titleEstrogen stimulates Th2 cytokine production and regulates the compartmentalisation of eosinophils during allergen challenge in a mouse model of asthma
dc.typeJournal article
local.bibliographicCitation.issue3
local.bibliographicCitation.lastpage260
local.bibliographicCitation.startpage252
local.contributor.affiliationCai, Yeping, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationZhou, Jiansheng, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationWebb, Dianne, College of Medicine, Biology and Environment, ANU
local.contributor.authoremailu4029322@anu.edu.au
local.contributor.authoruidCai, Yeping, u4029322
local.contributor.authoruidZhou, Jiansheng, u4032064
local.contributor.authoruidWebb, Dianne, u7700747
local.description.embargo2037-12-31
local.description.notesImported from ARIES
local.identifier.absfor110700 - IMMUNOLOGY
local.identifier.absfor119999 - Medical and Health Sciences not elsewhere classified
local.identifier.ariespublicationf5625xPUB1016
local.identifier.citationvolume158
local.identifier.doi10.1159/000331437
local.identifier.scopusID2-s2.0-84862803178
local.identifier.thomsonID000304485200006
local.identifier.uidSubmittedByf5625
local.type.statusPublished Version

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