Sex Hormones and Gender Differences in Asthma Pathophysiology
Summary
Asthma exhibits a clear pattern of sexual dimorphism: higher prevalence in boys during childhood switches to a female predominance from adolescence into adulthood. This shift parallels the onset of gonadal steroid production and underscores the influence of oestrogens, progesterone and androgens on airway biology. Oestrogen signalling via ERα, ERβ and G-protein-coupled receptors modulates type 2 (T2) inflammation by promoting eosinophil recruitment, mast cell activation and mucus hypersecretion. Progesterone-receptor engagement has context-dependent effects on cytokine profiles and airway smooth muscle tone, while androgens generally attenuate airway hyperresponsiveness and dampen pro-inflammatory cytokine release. Hormonal fluctuations across the menstrual cycle, pregnancy and menopause further alter symptom control and lung function, and exogenous hormone use in contraceptives or menopausal therapy can shift asthma risk. Interactions between sex steroids and sex-chromosome-linked genes integrate immunological, structural and neural pathways that govern airway calibre, remodelling and responsiveness. Recognition of these mechanisms is vital to advance precision medicine, guide hormone-based interventions and ensure that clinical trials account for sex as a critical determinant of asthma pathophysiology.
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Sex Hormones and Gender Differences in Asthma Pathophysiology publication trend
The graph below shows the total number of articles in sex hormones and gender differences in asthma pathophysiology across all publications each year (not limited to Nature Index journals).
Technical terms
Oestrogen: Primary female steroid hormone that modulates immune cell function, airway smooth muscle proliferation and mucus secretion via multiple receptor subtypes.
Progesterone: Female sex hormone that interacts with specific receptors to influence inflammatory mediators and bronchial tone, with effects dependent on receptor isoform and tissue context.
Androgens: Male steroid hormones, including testosterone, that generally attenuate airway hyperresponsiveness and pro-inflammatory cytokine release.
Type 2 (T2) inflammation: Immune response characterised by Th2 lymphocytes, eosinophils and cytokines (IL-4, IL-5, IL-13) that drive allergic airway inflammation and mucus hypersecretion.
Ovariectomy (OVX): Surgical removal of the ovaries in animal models to simulate a state of ovarian hormone deficiency.
References
- Exogenous female sex steroid hormones and new-onset asthma in women: a matched case–control study. BMC Medicine (2023).
- Systemic immunological responses are dependent on sex and ovarian hormone presence following acute inhaled woodsmoke exposure. Particle and Fibre Toxicology (2024).
- Sexual dimorphism in chronic respiratory diseases. Cell & Bioscience (2023).
- Estrogen Signaling Modulates Allergic Inflammation and Contributes to Sex Differences in Asthma. Frontiers in Immunology (2015).
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