Abstract

Pediatric obese asthma is a complex disease that remains poorly understood. The increasing worldwide incidence of both asthma and obesity over the last few decades, their current high prevalence and the challenges in treating obese asthmatic patients all highlight the importance of a better understanding of the pathophysiological mechanisms in obese asthma. While it is well established that patients with obesity are at an increased risk of developing asthma, the mechanisms by which obesity drives the onset of asthma, and modifies existing asthma, remain unclear. Here, we will focus on mechanisms by which obesity alters immune function in asthma. Lung parenchyma has an altered structure in some pediatric obese asthmatics, known as dysanapsis. Central adiposity is linked to reduced pulmonary function and a better predictor of asthma risk in children than BMI. Obesity in young children is associated with an increased risk of developing asthma, as well as early puberty, and hormonal alterations are implicated in obese asthma. Obesity and asthma each yield immunometabolic dysregulation separately and we are learning more about alterations in these pathways in pediatric obese asthma and the potential impact of bariatric surgery on those processes. The recent progress in clarifying the connections between childhood obesity and asthma and their combined impacts on immune function moves us closer to the goals of improved understanding of the pathophysiological mechanisms underpinning obese asthma and improved therapeutic target selection. However, this common inflammatory disease remains understudied, especially in children, and much remains to be learned.

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