Estrogen receptor-α signaling increases allergen-induced IL-33 release and airway inflammation.

Background: Group 2 innate lymphoid cells (ILC2) are stimulated by IL-33 to increase IL-5 and IL-13 production and airway inflammation. While sex hormones regulate airway inflammation, it remained unclear whether estrogen signaling through estrogen receptor-α (ER-α, Esr1) or ER-β (Esr2) increased ILC2-mediated airway inflammation. We hypothesize that estrogen signaling increases allergen-induced IL-33 release, ILC2 cytokine production, and airway inflammation.

Testosterone Decreases House Dust Mite-Induced Type 2 and IL-17A-Mediated Airway Inflammation.

As adults, women are twice as likely as men to have asthma; however, the mechanisms explaining this sexual dimorphism remain unclear. Increased type 2 cytokines and/or IL-17A, leading to increased airway eosinophils and neutrophils, respectively, are associated with asthma. Previous studies showed that testosterone, signaling through the androgen receptor (AR), decreased Th2-mediated allergic inflammation and type 2 innate immune responses during allergic inflammation.

Hormones, sex, and asthma.

Objective: To summarize the current literature on the sex disparity in asthma and the role of sex hormone signaling in allergic and neutrophilic airway inflammation.

Data Sources: PubMed and Centers for Disease Control and Prevention health surveys were searched.

Study Selections: Clinical and epidemiologic studies in children and adults as well as animal models of asthma were included in this review.

Testosterone Attenuates Group 2 Innate Lymphoid Cell-Mediated Airway Inflammation.

Sex hormones regulate many autoimmune and inflammatory diseases, including asthma. As adults, asthma prevalence is 2-fold greater in women compared to men. The number of group 2 innate lymphoid cells (ILC2) is increased in patients with asthma, and we investigate how testosterone attenuates ILC2 function.