Differential Effects of Testosterone and Estrogen on Inflammation and Disease Severity in Asthma and COPD
College
College of Arts and Sciences
Mentor Information
Narasaiah Kolluputi
Description
Asthma is a chronic inflammatory disease characterized by airway hyperresponsiveness, and airflow obstruction, while Chronic Obstructive Pulmonary Disease (COPD) is a progressive respiratory condition characterized by irreversible airflow limitation. Although previous research has examined hormonal influence, the specific effects of sex hormones in asthma and COPD remain unclear. This study aims to evaluate how testosterone and estrogen influence inflammation, disease severity and exacerbation frequency in adults with asthma and COPD. A comprehensive literature review using PubMed with keywords (asthma OR COPD) AND (sex hormones OR estrogen OR testosterone) AND (inflammation OR disease severity OR exacerbations) yielded 145 articles. After screening for human studies within the past five years and excluding non- English and irrelevant articles, 52 were included, covering cross-sectional, experimental, and randomized controlled studies on sex-based hormone effects in obstructive lung disease. The literature suggests higher testosterone is associated with better lung function and lower airway inflammation, with up to 41% lower odds of asthma and reduced COPD risk (OR ≈ 0.77). In contrast, estrogen signaling is associated with increased pro-inflammatory pathways, reduced lung function, and higher exacerbation risk. Hormonal imbalances, including low testosterone and menstrual-related changes, were associated with increased exacerbations, with up to 40% of women reporting worsened asthma symptoms during menstruation. These findings suggest sex hormones influence disease outcomes through immune mechanisms with estrogen driven Th2 inflammation and testosterone suppression of inflammatory pathways. Hormonal status can impact symptom control and treatment response. Future research should clarify why these differences exist biologically, beyond hormones or environment alone.
Differential Effects of Testosterone and Estrogen on Inflammation and Disease Severity in Asthma and COPD
Asthma is a chronic inflammatory disease characterized by airway hyperresponsiveness, and airflow obstruction, while Chronic Obstructive Pulmonary Disease (COPD) is a progressive respiratory condition characterized by irreversible airflow limitation. Although previous research has examined hormonal influence, the specific effects of sex hormones in asthma and COPD remain unclear. This study aims to evaluate how testosterone and estrogen influence inflammation, disease severity and exacerbation frequency in adults with asthma and COPD. A comprehensive literature review using PubMed with keywords (asthma OR COPD) AND (sex hormones OR estrogen OR testosterone) AND (inflammation OR disease severity OR exacerbations) yielded 145 articles. After screening for human studies within the past five years and excluding non- English and irrelevant articles, 52 were included, covering cross-sectional, experimental, and randomized controlled studies on sex-based hormone effects in obstructive lung disease. The literature suggests higher testosterone is associated with better lung function and lower airway inflammation, with up to 41% lower odds of asthma and reduced COPD risk (OR ≈ 0.77). In contrast, estrogen signaling is associated with increased pro-inflammatory pathways, reduced lung function, and higher exacerbation risk. Hormonal imbalances, including low testosterone and menstrual-related changes, were associated with increased exacerbations, with up to 40% of women reporting worsened asthma symptoms during menstruation. These findings suggest sex hormones influence disease outcomes through immune mechanisms with estrogen driven Th2 inflammation and testosterone suppression of inflammatory pathways. Hormonal status can impact symptom control and treatment response. Future research should clarify why these differences exist biologically, beyond hormones or environment alone.
