Because of the critical role of hydrophobic surfactant protein B (SP-B) in lung function, SP-B was researched in asthmatics to determine if it had a role in developing obesity-induced airway inflammation. For a study, the researchers sought to determine if obesity caused a change in circulating SP-B in adult asthmatics. Furthermore, 129 asthmatics were enrolled and divided into 3 groups (obese, overweight, and normal-weight groups) based on their Body mass index (BMI). The enzyme-linked immunosorbent assay was used to measure SP-B levels in the blood. The SFTPB gene was genotyped for 4 single nucleotide polymorphisms. Liquid chromatography-tandem mass spectrometry was used to determine serum ceramide levels. Obese people had significantly lower serum SP-B levels than the ones with heavy or average weight (P=.002). The blood SP-B level was strongly linked with serum levels of C18:0 ceramide and transforming growth factor-beta 1 and BMI (r=−0.200; r=−0.215; r=−0.332, P<.050 for all). In female asthmatics, there was an inverse relationship between serum SP-B and fractional exhaled nitric oxide levels (r=0.287, P=.009). Obesity and overweight people had a genetic tendency to the SFTPB gene at 9,306 A more than G. Obesity changed ceramide metabolism, resulting in pulmonary surfactant failure and delayed airway inflammation resolution, ultimately contributing to obese asthmatic phenotypes.