Obesity and asthma are global public health issues. Obesity-related asthma is a distinct asthma phenotype with complex pathogenesis, influenced by mechanical compression, inflammation, metabolism, gene regulation, and vitamin D deficiency. Weight loss treatments can benefit asthma, while changes in gut and airway microbial communities and their metabolites may contribute to obesity-related asthma. The Th17/Treg balance in gut microbiota regulates immune responses and host metabolism, and therapeutic measures related to gut microbiota diversity may improve chronic inflammation associated with obesity by regulating this balance. Early microbial diversity reduction predicts asthma development and allergy through Th2/Th1 imbalance. Short-chain fatty acids (SCFAs) regulate regulatory T cells, controlling immune homeostasis in the lungs to suppress allergic inflammation and weight gain. Understanding the microbial mechanisms of obesity-related asthma is crucial for clinical treatment. This review discusses the characteristics and pathogenesis of obesity-related asthma, its relationship with gut and airway microbiota, and current treatment measures. Obesity is a major risk factor for asthma in children and adults, with unclear mechanistic basis. Asthma is a heterogeneous disease with different phenotypes, and obesity and asthma are closely related and influence each other. Numerous studies show obesity is associated with increased asthma risk in adults and children. Rapid weight gain in the first two years of life is the strongest predictor of childhood asthma development. Asthma-related exercise intolerance and poor quality of life may contribute to more obesity. Studying the interaction of obesity and asthma is crucial. The Global Initiative for Asthma (GINA) identified obesity-related asthma as a special phenotype. Patients with this phenotype have obvious respiratory symptoms but not obvious airway eosinophilic inflammation. This phenotype is dominated by neutrophil infiltration, is not sensitive to inhaled corticosteroids, and is prone to developing refractory asthma. Obesity-related asthma increases the risk of hospitalization for severe disease and has poor efficacy with standard treatment. Obesity-related asthma includes two phenotypes: late-onset asthma with low inflammatory response and early-onset asthma with high allergic inflammatory response. Obesity is a risk factor for asthma, with increasing prevalence and incidence. In the U.S., asthma affects nearly 6.5 million children, and 15% are overweight, another 17% are obese. Obesity is recognized as a main risk factor for asthma, with studies showing obesity usually precedes asthma attacks. Obesity is associated with increased asthma severity and may begin in utero. A meta-analysis indicated maternal obesity and overweight during pregnancy are linked to increased asthma risk in offspring. Obesity-related asthma patients can significantly reduce asthma symptoms and airway hyperresponsiveness with weight loss. Obesity and asthma are closely related, with increasing evidence that asthma may also contribute to obesity. The relationship between obesity and asthma is complex, with obesity causing Th1 inflammation and Th1 inflammation being more intense in obese children with asthma. Obesity affects asthma in both individuals with and without allergies. Obesity-related asthma patients haveObesity and asthma are global public health issues. Obesity-related asthma is a distinct asthma phenotype with complex pathogenesis, influenced by mechanical compression, inflammation, metabolism, gene regulation, and vitamin D deficiency. Weight loss treatments can benefit asthma, while changes in gut and airway microbial communities and their metabolites may contribute to obesity-related asthma. The Th17/Treg balance in gut microbiota regulates immune responses and host metabolism, and therapeutic measures related to gut microbiota diversity may improve chronic inflammation associated with obesity by regulating this balance. Early microbial diversity reduction predicts asthma development and allergy through Th2/Th1 imbalance. Short-chain fatty acids (SCFAs) regulate regulatory T cells, controlling immune homeostasis in the lungs to suppress allergic inflammation and weight gain. Understanding the microbial mechanisms of obesity-related asthma is crucial for clinical treatment. This review discusses the characteristics and pathogenesis of obesity-related asthma, its relationship with gut and airway microbiota, and current treatment measures. Obesity is a major risk factor for asthma in children and adults, with unclear mechanistic basis. Asthma is a heterogeneous disease with different phenotypes, and obesity and asthma are closely related and influence each other. Numerous studies show obesity is associated with increased asthma risk in adults and children. Rapid weight gain in the first two years of life is the strongest predictor of childhood asthma development. Asthma-related exercise intolerance and poor quality of life may contribute to more obesity. Studying the interaction of obesity and asthma is crucial. The Global Initiative for Asthma (GINA) identified obesity-related asthma as a special phenotype. Patients with this phenotype have obvious respiratory symptoms but not obvious airway eosinophilic inflammation. This phenotype is dominated by neutrophil infiltration, is not sensitive to inhaled corticosteroids, and is prone to developing refractory asthma. Obesity-related asthma increases the risk of hospitalization for severe disease and has poor efficacy with standard treatment. Obesity-related asthma includes two phenotypes: late-onset asthma with low inflammatory response and early-onset asthma with high allergic inflammatory response. Obesity is a risk factor for asthma, with increasing prevalence and incidence. In the U.S., asthma affects nearly 6.5 million children, and 15% are overweight, another 17% are obese. Obesity is recognized as a main risk factor for asthma, with studies showing obesity usually precedes asthma attacks. Obesity is associated with increased asthma severity and may begin in utero. A meta-analysis indicated maternal obesity and overweight during pregnancy are linked to increased asthma risk in offspring. Obesity-related asthma patients can significantly reduce asthma symptoms and airway hyperresponsiveness with weight loss. Obesity and asthma are closely related, with increasing evidence that asthma may also contribute to obesity. The relationship between obesity and asthma is complex, with obesity causing Th1 inflammation and Th1 inflammation being more intense in obese children with asthma. Obesity affects asthma in both individuals with and without allergies. Obesity-related asthma patients have