Journal Scan Inflammation accelerates athero-sclerotic processes in obstructive sleep apnea syndrome (OSAS) - Quercioli A Sleep loss activates cellular markers of inflammation: sex differences-猫眼课题宝

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2012

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其他

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作者：

U. C. Ojha

可能的，摘要：睡眠障碍与炎症和相关疾病有关，包括心血管疾病、关节炎和糖尿病。鉴于炎症性疾病患病率的性别差异与女性的相关性更强，本研究旨在测试睡眠不足对促炎细胞因子活性的细胞机制的影响。在26名健康成人（11名女性; 15名男性）中，在基线期和部分睡眠剥夺后（从23：00至3.00 h清醒）的08：00、12：00、16：00、20：00和23：00 h重复评估单核细胞胞内促炎细胞因子的产生。在一夜睡眠不足后的早晨，单核细胞产生的白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）在两种性别之间有差异。而女性和男性都表现出显着增加的脂多糖（LPS）刺激的IL-6和TNF-α的生产后，立即在早晨PSD，生产这些细胞因子在傍晚和傍晚的女性增加相比，在男性减少。睡眠不足诱导单核细胞促炎细胞因子反应的功能改变，与男性的变化相比，女性显示出更大的细胞免疫激活。这些结果对于理解睡眠障碍在不同性别炎症性疾病风险特征中的作用具有意义。摘要：阻塞性睡眠呼吸暂停（OSA）的特点是经常性缺氧应激似乎在中性粒细胞粘附内皮细胞的增加以及前者向炎症区域的迁移中发挥作用。细胞间粘附分子1（ICAM-1）和白细胞介素（IL）-8是广泛用于OSA研究炎症的标志物。本研究的目的是使用特异性酶免疫分析（EIA）试剂盒检测12例肥胖OSA（OO）患者、10例非肥胖OSA（诺奥）患者、10例肥胖非OSA（ONO）患者和8例健康受试者（HS）的呼吸冷凝液、诱导痰中血浆和炎性细胞中ICAM-1和IL-8的水平。与健康受试者相比，在肥胖OSA患者、非肥胖OSA患者和肥胖非OSA受试者的诱导痰中观察到血浆和呼出的IL-8和ICAM浓度以及中性粒细胞百分比显著增加。然而，尽管发现这些炎症标志物在肥胖OSA患者中呈上升趋势，但在非肥胖OSA患者和肥胖非OSA受试者中均未观察到差异。最后，一个显着的睡眠剥夺已被证明增加大鼠血清和外周血单核细胞中的炎症标志物。炎症是与诸如肥胖、癌症和心血管疾病等病理学相关的病症。我们研究了大鼠不同部位白色脂肪组织中促炎和抗炎细胞因子和脂肪因子的变化。我们还评估了96小时睡眠剥夺后的血脂和血清皮质酮、瘦素和脂联素水平。方法：实验分为对照组（C组）和异相睡眠剥夺96 h组（PSD组）。将10只大鼠随机分配到对照组（C）或PSD组。完成PSD方案后，采集肠系膜（MEAT）和腹膜后（RPAT）脂肪组织、肝脏和血清。在MEAT和RPAT中分析白细胞介素（IL）-6、白细胞介素（IL）-10和肿瘤坏死因子（TNF）-α的水平，并分析血清中的瘦素、脂联素、葡萄糖、皮质酮和血脂水平。结果：PSD后，RPAT中IL-6水平升高，而MEAT中IL-6水平保持不变。IL-10蛋白浓度在两种贮库中均未改变，MEAT中TNF-α ±水平降低。PSD 96小时后，血清中葡萄糖、甘油三酯（TG）、VLDL和瘦素降低;脂联素未改变，皮质酮升高。结论：PSD可减少脂肪量，并可调节不同脂肪组织中细胞因子的含量。两种脂肪组织的炎症反应均减弱，RPAT中IL-6水平升高，MEAT中TNF-α ±蛋白浓度降低，血清中皮质酮水平升高。摘要目的：据报道，患有阻塞性睡眠呼吸暂停（OSA）的学龄儿童的N-末端B型利钠肽原（NT-proBNP）（心室张力的标志物）和C-反应蛋白（CRP）（炎症的标志物）升高。我们假设，心血管疾病的发病率影响循环标志物和他们的超声心动图和多导睡眠图（PSG）与OSA的幼儿。方法：我们通过多导睡眠图、超声心动图和血清CRP和NT-proBNP水平评估了因OSA接受腺样体扁桃体切除术（TA）的幼儿。研究结果：共纳入90名OSA儿童（平均年龄19 +/- 7个月; 71.2%为男性; BMI，z = 0.62 +/- 1.04）和45名年龄和性别匹配的对照。TA后3个月，对72名儿童重新评估NT-proBNP和CRP。OSA受试者的NT-proBNP水平（pg/mL）（189.1 ± 112.7）高于对照受试者（104.8 ± 49.5; P = .006）。TA后NT-proBNP（187.8 +/- 114 vs 86 +/- 32.6; P = 0.002）和CRP水平（mg %）（0.49 +/- 0.41 vs 0.1 +/- 0.17; P <0.05）均降低。多普勒脉搏波测量三尖瓣反流（TR），反映肺动脉高压，与CRP（r = 0.61，P <0.01）相关，但与NT-proBNP（r =-0.14，P = 0.53）水平无关。左室舒张末期内径（LVEDD）在最大正常范围（0.91

possible which ABSTRACT: Sleep disturbance is associated with inflammation and related disorders including cardiovascular disease, arthritis, and diabetes mellitus. Given sex differences in the prevalence of inflammatory disorders with stronger associations in females, this study was undertaken to test the effects of sleep loss on cellular mechanisms that contribute to proinflammatory cytokine activity. In 26 healthy adults (11 females; 15 males), monocyte intracellular proinflammatory cytokine production was repeatedly assessed at 08:00, 12:00, 16:00, 20:00, and 23:00h during a baseline period and after partial sleep deprivation (awake from 23:00 to 3.00h). In the morning after a night of sleep loss, monocyte production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) differentially changed between the two sexes. Whereas both females and males showed a marked increase in the lipopolysaccharide (LPS) - stimulated production of IL-6 and TNF-alpha in the morning immediately after PSD, production of these cytokines during the early- and late evening was increased in the females as compared to decreases in the males. Sleep loss induces a functional alteration of monocyte proinflammatory cytokine responses with females showing greater cellular immune activation as compared to changes in males. These results have implications for understanding the role of sleep disturbance in the differential risk profile for inflammatory disorders between the sexes. ABSTRACT: The recurrent hypoxic stress that characterizes obstructive sleep apnea (OSA) seems to play a role in the increased adherence of neutrophils to endothelial cells as well as in the resulting migration of the former to the inflamed area. Intercellular adhesion molecule 1 (ICAM-1) and interleukin (IL)-8 are markers widely used in OSA studies to investigate inflammation. The aim of this study was to measure ICAM-1 and IL-8 levels in the breath condensate and in the plasma and inflammatory cells in the induced sputum of 12 obese OSA (OO) patients, 10 nonobese OSA (NOO) patients, 10 obese non-OSA (ONO) subjects, and 8 healthy subjects (HS) using a specific enzyme immunoassay (EIA) kit. A significant increase in both plasma and exhaled IL-8 and ICAM concentrations and percentage neutrophils was observed in the induced sputum of obese OSA patients, non-obese OSA patients, and obese non-OSA subjects compared with healthy subjects. However, although these inflammatory markers were found to follow an upward trend in obese OSA patients no difference was observed in both either non-obese OSA patients and obese non-OSA subjects. Finally, a significant Sleep deprivation has been shown to increase inflammatory markers in rat sera and peripheral blood mononuclear cells. Inflammation is a condition associated with pathologies such as obesity, cancer, and cardiovascular diseases. We investigated changes in the pro and anti-inflammatory cytokines and adipokines in different depots of white adipose tissue in rats. We also assessed lipid profiles and serum levels of corticosterone, leptin, and adiponectin after 96 hours of sleep deprivation. METHODS: The study consisted of two groups: a control (C) group and a paradoxical sleep deprivation by 96 h (PSD) group. Ten rats were randomly assigned to either the control group (C) or the PSD. Mesenteric (MEAT) and retroperitoneal (RPAT) adipose tissue, liver and serum were collected following completion of the PSD protocol. Levels of interleukin (IL)-6, interleukin (IL)-10 and tumour necrosis factor (TNF)-Î± were analysed in MEAT and RPAT, and leptin, adiponectin, glucose, corticosterone and lipid profile levels were analysed in serum. RESULTS: IL-6 levels were elevated in RPAT but remained unchanged in MEAT after PSD. IL-10 protein concentration was not altered in either depot, and TNF-Î± levels decreased in MEAT. Glucose, triglycerides (TG), VLDL and leptin decreased in serum after 96 hours of PSD; adiponectin was not altered and corticosterone was increased. CONCLUSIONS: PSD decreased fat mass and may modulate the cytokine content in different depots of adipose tissue. The inflammatory response was diminished in both depots of adipose tissue, with increased IL-6 levels in RPAT and decreased TNF-Î ± protein concentrations in MEAT and increased levels of corticosterone in serum. ABSTRACT OBJECTIVE: N-terminal pro-B-type natriuretic peptide (NT-proBNP), a marker of ventricular strain, and C-reactive protein (CRP), a marker of inflammation, are reportedly elevated in school-aged children with obstructive sleep apnea (OSA). We hypothesized that cardiovascular morbidity affects circulating markers and their echocardiographic and polysomnographic (PSG) correlates in young children with OSA. METHODS: We assessed young children undergoing adenotonsillectomy (TA) for OSA by polysomnography, echocardiography, and serum CRP and NT-proBNP levels. RESULTS: A total of 90 children with OSA (mean age 19 +/- 7 months; 71.2% male; BMI, z = 0.62 +/- 1.04) and 45 age- and sex-matched controls were included. Three months following TA, 72 children were reassessed for NT-proBNP and CRP. NT-proBNP level (pg/mL) was higher in subjects with OSA (189.1 +/- 112.7) vs control subjects (104.8 +/- 49.5; P = .006). Both NT-proBNP (187.8 +/- 114 vs 86 +/- 32.6; P = .002) and CRP levels (mg %) (0.49 +/- 0.41 vs 0.1 +/- 0.17; P < .05) decreased following TA. Doppler pulse wave measuring tricuspid regurgitation (TR), a reflection of pulmonary hypertension, correlated with CRP (r = 0.61, P < .01) but not NT-proBNP (r = -0.14, P = .53) levels. Left ventricle end-diastolic diameter (LVEDD) was at the maximal normal range (0.91

Journal Scan Inflammation accelerates athero-sclerotic processes in obstructive sleep apnea syndrome (OSAS) - Quercioli A Sleep loss activates cellular markers of inflammation: sex differences

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