Contribution of systemic and airway immune responses to pediatric obesity-related asthma

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 naive 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. (C) 2020 Elsevier Ltd. All rights reserved.

Automated summary

Childhood obesity is associated with complex immune response differences in asthma, including non-allergic or non-T2 phenotypes and allergic Th cell responses. Evidence suggests that genetic and epigenetic mechanisms play a role in these immune responses, and may provide insights for the development of targeted therapies for obesity-related asthma.