HUNTINGTON, W.Va. — Researchers at Marshall University have identified a potential immune mechanism contributing to metabolic dysfunction and insulin resistance associated with obstructive sleep apnea (OSA), offering new insight into how chronic sleep-related oxygen deprivation affects overall health. 

The study, published in April 2026 in SLEEP, focused on intermittent hypoxia, which is repeated drops in oxygen levels that occur during episodes of obstructive sleep apnea, and its impact on inflammation within metabolic organs such as visceral fat tissue and the liver. Researchers found that specific immune cells known as CD11b+ monocytes and macrophages appear to play a significant role in driving inflammation and metabolic dysfunction linked to OSA. 

Using a mouse model designed to mimic the intermittent oxygen deprivation experienced in sleep apnea, investigators selectively and systematically depleted CD11b+ immune cells and evaluated the resulting metabolic changes. 

The results showed that depletion of these inflammatory immune cells significantly improved insulin sensitivity and attenuated metabolic dysfunction in mice exposed to intermittent hypoxia. In addition, reduced infiltration of inflammatory cells was observed in visceral white adipose tissue and the liver. These changes were accompanied by decreases in biomarkers of chronic inflammation and cellular senescence, suggesting a key role for CD11b⁺ immune cells in mediating intermittent hypoxia–induced metabolic impairment. 

“These findings help us better understand the biological mechanisms linking obstructive sleep apnea to metabolic disease,” said Abdelnaby Khalyfa, M.Sc., Ph.D., professor of biomedical sciences at the Joan C. Edwards School of Medicine and lead author on the study. “By identifying the role these immune cells play in inflammation and insulin resistance, we may be able to develop more targeted anti-inflammatory therapies aimed at reducing long-term complications associated with sleep apnea.” 

 The study also identified reductions in senescence-associated secretory phenotype (SASP) markers, including p16 and IL-16, following depletion of CD11b+ cells, suggesting these immune cells may contribute to chronic inflammatory signaling and accelerated biological aging in metabolic tissues. 

 According to the research team, the findings support continued investigation into therapies targeting inflammatory immune responses in patients with obstructive sleep apnea. 

The study was conducted by a team of investigators, including Khalyfa, Sarfraz Ahmed, Ph.D., Rajan Lamichhane, Ph.D., and David Gozal, M.D., M.B.A., Ph.D. (Hon) from Marshall University and Zhuanhong Qiao, Ph.D., of the University of Missouri. This study was supported by unrestricted start-up funds awarded to Khalyfa by the Joan C. Edwards School of Medicine through the Marshall University Research Corporation (MURC), Huntington, West Virginia, USA. Gozal is supported in part by NIH grants HL166617 and HL169266. This research was also supported in part by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number P20GM103434, through the West Virginia IDeA Network of Biomedical Research Excellence (WV-INBRE). 

The full study may be found at https://doi.org/10.1093/sleep/zsag117.  

Date Posted: Friday, June 19, 2026