Abstract
Childhood obesity contributes to many diseases, including asthma. Although the precise mechanism by which obesity causes asthma is not known, there is literature to suggest that innate and adaptive systemic and airway immune responses in obese children with asthma differ from those in normal-weight children with asthma. Both non-allergic or non-T2 phenotype with systemic T helper (Th)1 polarization and allergic Th cell responses have been reported in childhood obesity-related asthma. There is preliminary evidence to suggest that genetic and epigenetic mechanisms contribute to these immune responses. Initial investigations into the biology of non-T2 immune responses have identified upregulation of genes in the CDC42 pathway. CDC42 is a RhoGTPase that plays a key role in Th cell physiology, including preferential naïve Th cell differentiation to Th1 cells, as well as cytokine production and exocytosis. These novel pathways are promising findings to direct targeted therapy development for obesity-related asthma to address the disease burden.