As the incidence of obesity-associated diseases continues to rise at a staggering rate, the need for a better understanding of the molecular mechanisms that regulate metabolic-immunological crosstalk during obesity has risen to the forefront of biomedical investigation. Obesity is a proven risk factor for allergic airway diseases-such as asthma. Asthma severity appears to be increased in the obese and alters the response to controller therapy leading to greater healthcare utilization and a reduced quality of life. Various mechanism accounts for unravelling the intricacies of obesity-induced or obesity-exacerbated asthma. However, our current knowledge on how myeloid progenitor cells and dendritic cell subsets modulate inflammation and the development of asthma in obesity is limited. Our lab investigate novel endogenous signaling pathways and druggable targets in progenitor cells related to adaptive immunity that regulates airway inflammation in obesity.
