‘These findings help us better understand the biological mechanisms linking obstructive sleep apnea to metabolic disease.’
Key takeaways:
- Researchers identified specific immune cells, CD11b+ monocytes and macrophages, as key drivers of inflammation in metabolic organs like the liver and visceral fat during intermittent hypoxia.
- In a mouse model, systematically depleting these immune cells improved insulin sensitivity, reduced inflammatory cell infiltration, and decreased markers of cellular senescence.
- The findings suggest that targeting these immune mechanisms could lead to new anti-inflammatory therapies for reducing long-term metabolic complications in patients with obstructive sleep apnea.
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 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,” says Abdelnaby Khalyfa, MSc, PhD, professor of biomedical sciences at the Joan C. Edwards School of Medicine and lead author on the study, in a release. “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 the depletion of CD11b+ cells. This suggests 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 OSA.
The study was conducted by a team of investigators, including Khalyfa, Sarfraz Ahmed, PhD, Rajan Lamichhane, PhD, and David Gozal, MD, MBA, PhD (Hon) from Marshall University, and Zhuanhong Qiao, PhD, of the University of Missouri.
