Leptin secreted by adipocytes under obese conditions binds to the leptin receptor (obR) on the surface of macrophages, activates the JNK/STAT3/Akt signaling pathway, drives the polarization of macrophages toward the pro-inflammatory M1 phenotype, and releases chemokines such as CXCL2, thereby recruiting a large number of neutrophils to the airways and ultimately exacerbating obesity-related neutrophilic airway inflammation. This evidence concerns the gene LEPR and obesity due to melanocortin 4 receptor deficiency.