Sleep medicine · 2025
Plasma IL-22 and Claudin-4 in obstructive sleep apnea: A pilot observational study linking mucosal barrier biomarkers to disease severity.
СтатьяНаблюдательное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Liu Dan, Wang Yan, Wang Zhiding, Feng Jing
Аннотация
BACKGROUND: Obstructive sleep apnea (OSA) is characterized as a low-grade inflammatory condition resulting from injury induced by intermittent hypoxia (IH). Interleukin-22 (IL-22), a mucosa-targeting cytokine, regulates tight junction proteins like Claudin-4 (CLDN4) to enhance barrier function, yet its role in OSA remains underexplored.
METHODS: This pilot observational study included consecutive patients who underwent polysomnography. Plasma IL-22 and CLDN4 levels were measured using an enzyme-linked immunosorbent assay. Rat models of IH-exposed colon tissues were used for histology and immunohistochemical analysis. All statistical analyses were performed using SPSS 20.0.
RESULTS: The expression of plasma IL-22 and CLDN4 was found to be positively correlated in OSA patients (r = 0.512, p < 0.001). Plasma IL-22 and CLDN4 levels exhibited a significant positive correlation with the apnea-hypopnea index (both p < 0.001), arousal index (p = 0.001 and p = 0.014), oxygen desaturation index (p < 0.001 and p = 0.001), and T90 (r = 0.379, p < 0.001 and p = 0.002). They also exhibited significant negative correlations with sleep efficiency (0.029; p = 0.004), REM sleep phases (p = 0.037 and p = 0.015), and mean oxygen saturation (SpO2) (p = 0.044 and p = 0.006). Plasma IL-22 and CLDN4 were significantly increased in the OSA group (p < 0.001), especially in severe OSA. The diagnostic value of plasma IL-22 combined with CLDN4 was superior to that of other indicators, with an AUC of 0.849 (0.783-0.915) for diagnosing OSA and an AUC of 0.909 (0.856-0.961) for diagnosing severe OSA. Pathological staining of the rat colon confirmed the damage of intermittent hypoxia (IH) to the intestine. The rat IH group had more IL-22 in the intestinal lymph node and more CLDN4 in the intestinal epithelium than the normal control (NC) group. The expression trends of IL-22 and CLDN4 in rat plasma were consistent with those observed in tissue samples.
CONCLUSION: Plasma IL-22 and CLDN4 were associated with OSA severity and mucosal barrier alterations. Their co-regulation aligns with preclinical models of IH-driven barrier adaptation, supporting further mechanistic investigation. The diagnostic potential of the IL-22 +CLDN4 panel warrants validation in larger patient cohorts.
METHODS: This pilot observational study included consecutive patients who underwent polysomnography. Plasma IL-22 and CLDN4 levels were measured using an enzyme-linked immunosorbent assay. Rat models of IH-exposed colon tissues were used for histology and immunohistochemical analysis. All statistical analyses were performed using SPSS 20.0.
RESULTS: The expression of plasma IL-22 and CLDN4 was found to be positively correlated in OSA patients (r = 0.512, p < 0.001). Plasma IL-22 and CLDN4 levels exhibited a significant positive correlation with the apnea-hypopnea index (both p < 0.001), arousal index (p = 0.001 and p = 0.014), oxygen desaturation index (p < 0.001 and p = 0.001), and T90 (r = 0.379, p < 0.001 and p = 0.002). They also exhibited significant negative correlations with sleep efficiency (0.029; p = 0.004), REM sleep phases (p = 0.037 and p = 0.015), and mean oxygen saturation (SpO2) (p = 0.044 and p = 0.006). Plasma IL-22 and CLDN4 were significantly increased in the OSA group (p < 0.001), especially in severe OSA. The diagnostic value of plasma IL-22 combined with CLDN4 was superior to that of other indicators, with an AUC of 0.849 (0.783-0.915) for diagnosing OSA and an AUC of 0.909 (0.856-0.961) for diagnosing severe OSA. Pathological staining of the rat colon confirmed the damage of intermittent hypoxia (IH) to the intestine. The rat IH group had more IL-22 in the intestinal lymph node and more CLDN4 in the intestinal epithelium than the normal control (NC) group. The expression trends of IL-22 and CLDN4 in rat plasma were consistent with those observed in tissue samples.
CONCLUSION: Plasma IL-22 and CLDN4 were associated with OSA severity and mucosal barrier alterations. Their co-regulation aligns with preclinical models of IH-driven barrier adaptation, supporting further mechanistic investigation. The diagnostic potential of the IL-22 +CLDN4 panel warrants validation in larger patient cohorts.