4 Autoimmune Disease-Related Cytokines May Be Controlled by OSA Airways Treatment

Airways therapy for patients with obstructive sleep apnea (OSA) appears to control aberrant levels of 4 cytokines involved in autoimmune disease and immune processes, according to a new study.

“OSA damages the health of 35% of adult Americans,” the researchers wrote. “Disordered sleep results in increased risk of several autoimmune disorders, but the molecular links to autoimmunity are poorly understood.”

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The study included 19 patients receiving nightly airways therapy for OSA: 18 reported using continuous positive airway pressure, while 1 used a dental airways device. Additionally, 19 patients with apnea receiving no airways therapy and 8 control subjects participated. 

“The control group was considerably younger and leaner, and potentially represented more nearly optimal biometric data and cytokine levels,” the researchers reported.

Levels of the cytokines A proliferation-inducing ligand (APRIL), CD30, interleukin-2 (IL-2), and interferon-α-2 (IFN α-2) differed significantly among airways-treated patients compared with untreated patients, according to the study. Among patients receiving airways-therapy, APRIL was 5.2-fold lower, CD30 was 1.6-fold higher,  IL-2 was 1.9-fold higher, and IFN α-2 was 2.9-fold higher than among untreated patients.

Levels of the cytokines among patients receiving airways therapy were more similar to levels among control subjects than among patients with untreated OSA, the researchers noted. 

“Our findings suggest the levels of these 4 cytokines may be altered by disordered sleep and perhaps by chronic hypoxia,” the researchers wrote. “Airways therapy of OSA patients appears to be an effective way to control aberrant levels of these four cytokines involved in autoimmune disease and immune processes.”

—Jolynn Tumolo

Reference:

Phillips BG, Wang Y, Ambati S, Ma P, Meagher RB. Airways therapy of obstructive sleep apnea dramatically improves aberrant levels of soluble cytokines involved in autoimmune disease. Clin Immunol. 2020;221:108601. doi:10.1016/j.clim.2020.108601