L. Nosetti, Claudio Tirelli, F. Marino, M. Gaiazzi, Lucia Sacchi, Mara De Amici, F. Barocci, R. Maio, M. Cosentino, Luigi Nespoli
{"title":"细胞因子与儿童期阻塞性睡眠呼吸暂停:一组儿童的研究","authors":"L. Nosetti, Claudio Tirelli, F. Marino, M. Gaiazzi, Lucia Sacchi, Mara De Amici, F. Barocci, R. Maio, M. Cosentino, Luigi Nespoli","doi":"10.3390/biologics4010004","DOIUrl":null,"url":null,"abstract":"Introduction: Obstructive Sleep Apnea (OSA) in children is characterized by repeated episodes of partial or complete obstruction of the upper airways that impair normal ventilation and cause hypoxia and sleep disruption. These episodes activate innate and adaptive immunity resulting in the production of proinflammatory cytokines: IL-1β, IL-6, TNF-α, and reactive oxygen species. The hypothalamic–pituitary–adrenal (HPT) axis is also activated with alteration of the circadian rhythm of cortisol synthesis. OSA in children, and even more in adults, induces a systemic inflammatory condition that contributes to the genesis of clinical complications: poor growth, learning disabilities, cardiovascular changes, insulin resistance, and metabolic syndrome. Methods: A total of 42 non-obese children (age 1–15 years) were enrolled among those sent to our sleep center to perform full polysomnography (PSG). After PSG, 6 children did not show OSA (controls), 20 had mild OSA (m OSA), and 16 had medium-severe OSA (MS OSA). In vitro IL-1β, TNF-α, and serum cortisol levels were measured at 2 and 8 am in the analyzed groups. Results: Cortisol levels did not differ between controls and OSA children. At 2 am, there were no differences between controls and OSA in TNF-α production, whereas at 8 am, TNF-α was reduced in MS-OSA. IL-1β production showed no differences between OSA and controls. Conclusions: In our population, only TNF-α production is suppressed in MS-OSA: this might indicate a role of OSA severity in inducing inflammation. In adults, the phenomenon is more pronounced due to the habitual greater severity/duration of OSA, presence of comorbidities (cardiovascular and metabolic), and different immune system function.","PeriodicalId":505652,"journal":{"name":"Biologics","volume":"39 2","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cytokines and Obstructive Sleep Apnea in Childhood: Study of a Group of Children\",\"authors\":\"L. Nosetti, Claudio Tirelli, F. Marino, M. Gaiazzi, Lucia Sacchi, Mara De Amici, F. Barocci, R. Maio, M. Cosentino, Luigi Nespoli\",\"doi\":\"10.3390/biologics4010004\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction: Obstructive Sleep Apnea (OSA) in children is characterized by repeated episodes of partial or complete obstruction of the upper airways that impair normal ventilation and cause hypoxia and sleep disruption. These episodes activate innate and adaptive immunity resulting in the production of proinflammatory cytokines: IL-1β, IL-6, TNF-α, and reactive oxygen species. The hypothalamic–pituitary–adrenal (HPT) axis is also activated with alteration of the circadian rhythm of cortisol synthesis. OSA in children, and even more in adults, induces a systemic inflammatory condition that contributes to the genesis of clinical complications: poor growth, learning disabilities, cardiovascular changes, insulin resistance, and metabolic syndrome. Methods: A total of 42 non-obese children (age 1–15 years) were enrolled among those sent to our sleep center to perform full polysomnography (PSG). After PSG, 6 children did not show OSA (controls), 20 had mild OSA (m OSA), and 16 had medium-severe OSA (MS OSA). In vitro IL-1β, TNF-α, and serum cortisol levels were measured at 2 and 8 am in the analyzed groups. Results: Cortisol levels did not differ between controls and OSA children. At 2 am, there were no differences between controls and OSA in TNF-α production, whereas at 8 am, TNF-α was reduced in MS-OSA. IL-1β production showed no differences between OSA and controls. Conclusions: In our population, only TNF-α production is suppressed in MS-OSA: this might indicate a role of OSA severity in inducing inflammation. 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引用次数: 0
摘要
导言:儿童阻塞性睡眠呼吸暂停(OSA)的特点是反复发作的上呼吸道部分或完全阻塞,影响正常通气,导致缺氧和睡眠障碍。这些发作会激活先天性和适应性免疫,导致促炎细胞因子的产生:IL-1β、IL-6、TNF-α 和活性氧。下丘脑-垂体-肾上腺(HPT)轴也会随着皮质醇合成昼夜节律的改变而被激活。儿童的 OSA 会诱发全身性炎症,成人的情况更为严重,从而导致临床并发症:发育不良、学习障碍、心血管变化、胰岛素抵抗和代谢综合征。研究方法在被送往睡眠中心进行全面多导睡眠图检查的儿童中,共选取了 42 名非肥胖儿童(1-15 岁)。PSG检查后,6名儿童未发现OSA(对照组),20名儿童患有轻度OSA(m OSA),16名儿童患有中重度OSA(MS OSA)。分析组分别在凌晨 2 点和 8 点测量了体外 IL-1β、TNF-α 和血清皮质醇水平。结果显示对照组和 OSA 儿童的皮质醇水平没有差异。凌晨2点,TNF-α的产生在对照组和OSA之间没有差异,而在早晨8点,TNF-α在MS-OSA中有所减少。IL-1β的产生在OSA和对照组之间没有差异。结论在我们的人群中,只有 TNF-α 的产生在 MS-OSA 中受到抑制:这可能表明 OSA 的严重程度在诱发炎症方面起了作用。在成人中,这种现象更为明显,原因是OSA的习惯性严重程度/持续时间更长、存在合并症(心血管和代谢)以及免疫系统功能不同。
Cytokines and Obstructive Sleep Apnea in Childhood: Study of a Group of Children
Introduction: Obstructive Sleep Apnea (OSA) in children is characterized by repeated episodes of partial or complete obstruction of the upper airways that impair normal ventilation and cause hypoxia and sleep disruption. These episodes activate innate and adaptive immunity resulting in the production of proinflammatory cytokines: IL-1β, IL-6, TNF-α, and reactive oxygen species. The hypothalamic–pituitary–adrenal (HPT) axis is also activated with alteration of the circadian rhythm of cortisol synthesis. OSA in children, and even more in adults, induces a systemic inflammatory condition that contributes to the genesis of clinical complications: poor growth, learning disabilities, cardiovascular changes, insulin resistance, and metabolic syndrome. Methods: A total of 42 non-obese children (age 1–15 years) were enrolled among those sent to our sleep center to perform full polysomnography (PSG). After PSG, 6 children did not show OSA (controls), 20 had mild OSA (m OSA), and 16 had medium-severe OSA (MS OSA). In vitro IL-1β, TNF-α, and serum cortisol levels were measured at 2 and 8 am in the analyzed groups. Results: Cortisol levels did not differ between controls and OSA children. At 2 am, there were no differences between controls and OSA in TNF-α production, whereas at 8 am, TNF-α was reduced in MS-OSA. IL-1β production showed no differences between OSA and controls. Conclusions: In our population, only TNF-α production is suppressed in MS-OSA: this might indicate a role of OSA severity in inducing inflammation. In adults, the phenomenon is more pronounced due to the habitual greater severity/duration of OSA, presence of comorbidities (cardiovascular and metabolic), and different immune system function.