Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, United States.
Department of Pediatrics, George Washington University, School of Medicine and Health Sciences, United States.
Paediatr Respir Rev. 2021 Mar;37:3-9. doi: 10.1016/j.prrv.2020.02.005. Epub 2020 Mar 6.
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.
儿童肥胖会导致许多疾病，包括哮喘。虽然肥胖导致哮喘的确切机制尚不清楚，但有文献表明，肥胖哮喘儿童与正常体重哮喘儿童的固有和适应性全身及气道免疫反应不同。在儿童肥胖相关哮喘中，已报道存在非过敏性或非 T2 表型伴全身辅助性 T 细胞（Th）1 极化和过敏性 Th 细胞反应。有初步证据表明，遗传和表观遗传机制有助于这些免疫反应。对非 T2 免疫反应生物学的初步研究已经确定了 CDC42 途径中基因的上调。CDC42 是一种 RhoGTPase，在 Th 细胞生理学中发挥关键作用，包括优先将幼稚 Th 细胞分化为 Th1 细胞，以及细胞因子的产生和胞吐作用。这些新的途径是有前途的发现，可以指导针对肥胖相关哮喘的靶向治疗开发，以解决疾病负担。
