Inflammation biomarkers in OSA, chronic obstructive pulmonary disease, and chronic obstructive pulmonary disease/OSA overlap syndrome

The present study shows that serum levels of the inflammatory markers IL-6, hs-CRP, and G-CSF are increased in patients with COPD and OVS compared with healthy controls. Furthermore, levels of IL-6, hs-CRP, and G-CSF were higher in participants with COPD and OVS compared with OSA alone. Second, we showed that participants with OVS have higher systemic inflammation levels as measured by leukocytes and neutrophils levels than COPD and OSA alone. Third, we observed no major impact of PAP therapy on cytokine levels in OSA.

Chronic low-grade inflammation is associated with the initiation and progression of atherosclerotic disease, heart failure, and obesity-related metabolic disorders. In the past 20 years, there has been an increased understanding of the role the innate immune response pathway plays in the development of vascular diseases through biomarkers such as IL-1, IL-6, and CRP CRP is an important serum inflammation marker. It is synthesized by the liver, and its production is mostly controlled by the proinflammatory cytokine IL-6. IL-6 is a circulating cytokine known to be secreted from a number of different cells, including activated macrophages, lymphocytes, and adipocytes Inflammation is the main stimulus for IL-6 production, but other stimuli also exist, such as cigarette smoke and adiposity Given that an elevated neutrophil-to-lymphocyte ratio is considered indicative of a state of subclinical systemic inflammation in chronic diseases, our data confirm that OSA, COPD, and OVS exhibit a profile of subclinical inflammatory states (with the latter being primarily driven by the COPD component) The higher neutrophil-to-lymphocyte ratio in COPD compared with OVS could be explained by the lower levels of lymphocytes observed in COPD. The present findings corroborate existing literature that suggests a link between the occurrence of COPD and a decrease in lymphocyte levels. Our linear regression model controlled for the effect of FEV₁, so we do not believe that the more severe pulmonary impairment in OVS, as indicated by a lower FEV₁ value of 53% compared to 63% in COPD, is necessarily driving the differences in cytokine levels observed between these 2 groups.

https://jcsm.aasm.org/doi/full/10.5664/jcsm.10600