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Obesity is linked to worse asthma symptoms. Epigallocatechin-3-gallate (EGCG) reduces airway inflammation, but no study investigated the effects of EGCG on obesity-associated asthma. We aimed here to evaluate the effects of EGCG on allergen-induced airway inflammation in high-fat diet-fed mice. Male C57Bl/6 mice maintained on either standard-chow or high-fat diet for 12 weeks were treated or not with EGCG (10 mg/kg/day, gavage, two weeks). Animals were intranasally challenged with ovalbumin (OVA). In lung tissue and bronchoalveolar lavage fluid (BALF), cell counting and markers of inflammation and oxidative stress were evaluated. High-fat diet-fed mice exhibited significantly higher body weight and epididymal fat mass compared with lean group. EGCG treatment reduced by 20% the epididymal fat mass in obese mice (P < 0.05). The OVA-induced increases of total cells and eosinophils in lung tissue of obese mice were significantly reduced EGCG treatment. The increased levels of TNF-α, IL-4, IL-5 and eotaxin in BALF of obese mice were normalized by EGCG. Likewise, the enhanced expression of inducible nitric oxide synthase (iNOS) and nitric oxide metabolite (NOx) levels in obese mice were normalized by EGCG. Reactive-oxygen species (ROS) and superoxide dismutase (SOD) levels were elevated and reduced, respectively, in lung tissue of obese mice, both of which were restored by EGCG. In lean mice, EGCG had no significant effect in evaluated parameter (body measures, and inflammatory and oxidative markers). EGCG turns to normal the levels of inflammatory and oxidative stress markers in lungs of obese mice, suggesting it could be an option to attenuate obesity-related asthma.Epigallocatechin-3-gallate (EGCG) reduces allergen-induced eosinophil infiltration in lung tissue of obese and asthmatic mice.EGCG turns to normal the levels of inflammatory and oxidative stress markers in lungs of obese and asthmatic mice.EGCG could be an option to attenuate obesity-related asthma.