Cytokine production from peripheral blood mononuclear cells and polymorphonuclear leukocytes in patients studied for suspected obstructive sleep apnea

Guasti, Luigina; Marino, Franca; Cosentino, Marco; Maroni, Lorenzo; Maresca, Andrea Maria; Colombo, Fausto; Maio, Ramòna Consuèlo; Castiglioni, Luana; Saporiti, Federica; Loraschi, Anna; Gaudio, Giovanni; Bernasconi, Antonella; Laurita, Emanuela; Grandi, Anna Maria; Venco, Achille

doi:10.1007/s11325-009-0315-x

Cited by 24 publications

(16 citation statements)

References 49 publications

(79 reference statements)

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“…Carniero et al 2009 [63] had a very small sample population (7) and showed that CPAP usage over 3 months decreases serum TNF-α, though not significantly. Guasti et al 2009 [74] also had a small sample population (only 16) and many of the patients had other comorbidities, such as elevated BMI. In addition to a small sample population (16) and patients having high BMIs, Vgontzas and colleagues [78] noted that there were discrepancies in the compliance of the patients using CPAP.…”

Section: Discussionmentioning

confidence: 99%

Treatment for sleep apnea by continuous positive airway pressure improves levels of inflammatory markers - a meta-analysis

et al. 2013

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BackgroundObstructive sleep apnea (OSA) is associated with coronary artery disease (CAD). Intermittent hypoxia associated with OSA increases sympathetic activity and may cause systemic inflammation, which may contribute to CAD in patients with OSA. Treatment with continuous positive airway pressure (CPAP) has been shown to change levels of inflammatory markers. We analyzed data from published studies by a systematic meta-analysis.ObjectiveTo asses if treatment for sleep apnea by CPAP will affect levels of inflammatory markers.Data resourcesPubMed, Embase and Cochrane library.MethodsStudy eligibility criteria full text English studies of adult, human subjects, addressing values of at least one of the inflammatory markers before and after CPAP treatment. We used the definition of OSA as an apnea-hypopnea index (AHI) of ≥ 5/h, reported values in mean and standard deviation or median with range.ParticipantsAdult, human.InterventionsCPAP treatment for OSA.Study appraisal and synthesis methodA total of 3835 studies were reviewed for inclusion, while 23 studies pooled for analysis. A total of 14 studies with 771 patients were pooled for C-reactive protein (CRP); 9 studies with 209 patients were pooled for tumor necrosis factor-alpha (TNF-α); and 8 studies with 165 patients were pooled for interleukin-6 (IL-6).Endpoint definitionsThe following inflammatory markers were chosen: CRP, TNF-α, and IL-6.ResultsC-reactive protein: Study level means ranged from 0.18 to 0.85 mg/dl before CPAP treatment and 0.10 to 0.72 mg/dl after CPAP treatment. Mean differences, at a study level, ranged from −0.05 to 0.50. The pooled mean difference was 0.14 [95% confidence interval 0.08 to 0.20, p < 0.00001]. There was heterogeneity in this endpoint (df = 13, p < 0.00001, I2 = 95%).Tumor necrosis factor-α: Study level means ranged from 1.40 to 50.24 pg/ml before CPAP treatment and 1.80 to 28.63 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from −1.23 to 21.61. The pooled mean difference was 1.14 [95% confidence interval 0.12 to 2.15, p = 0.03]. There was heterogeneity in this endpoint (df = 8, p < 0.00001, I2 = 89%).Interleukin-6: Study level means ranged from 1.2 to 131.66 pg/ml before CPAP treatment and 0.45 to 66.04 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from −0.40 to 65.62. The pooled mean difference was 1.01 [95% confidence interval −0.00 to 2.03, p = 0.05]. There was heterogeneity in this endpoint (df = 7, p < 0.00001, I2 = 95%).LimitationsOnly published data. Studies pooled were mainly small, non-randomized trials.ConclusionSleep apnea treatment with CPAP improves levels of inflammatory markers.

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Section: Discussionmentioning

confidence: 99%

Treatment for sleep apnea by continuous positive airway pressure improves levels of inflammatory markers - a meta-analysis

et al. 2013

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“…There was heterogeneity in this endpoint (df (Q) 31, p < 0.0001, I 2 = 96.4) (Figure 1). [56][57][58][59][60][61][62][63][64][65][66][67][68] The second analysis was performed with studies reporting OSA patients in groups (mild, moderate, or severe): standardized mean difference ranged from -0.18 to 8.59. The pooled mean difference was calculated to be 1.07 (LL 0.60 to UL 1.54, p < 0.0001).…”

Section: C-reactive Proteinmentioning

confidence: 99%

Serum Inflammatory Markers in Obstructive Sleep Apnea: A Meta-Analysis

Nadeem

Molnár

Madbouly

et al. 2013

Journal of Clinical Sleep Medicine

370

308

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“…Snoring is associated with cytokine release from blood cells, and promotes inflammation [90]. Snoring involves vibration of the soft palate, pharyngeal walls, epiglottis and the tongue, and causes lesions of the UA mucosa, pharyngeal muscles, and their innervating nerves [91][92][93].…”

Section: Hypothermia and Inflammationmentioning

confidence: 99%

Dysfunctional Nucleus Tractus Solitarius: Its Crucial Role in Promoting Neuropathogentic Cascade of Alzheimer’s Dementia—A Novel Hypothesis

Daulatzai

2012

Neurochem Res

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The pathophysiological mechanism(s) underlying Alzheimer's disease (AD) still remain unclear, and no disease-modifying or prophylactic therapies are currently available. Unraveling the fundamental neuropathogenesis of AD is an important challenge. Several studies on AD have suggested lesions in a number of CNS areas including the basal forebrain, hippocampus, entorhinal cortex, amygdale/insula, and the locus coeruleus. However, plausible unifying studies on the upstream factors that involve these heterogeneous regions and herald the onset of AD pathogenesis are not available. The current article presents a novel nucleus tractus solitarius (NTS) vector hypothesis that underpins several disparate biological mechanisms and neural circuits, and identifies relevant hallmarks of major presumptive causative factor(s) linked to the NTS, in older/aging individuals. Aging, obesity, infection, sleep apnea, smoking, neuropsychological states, and hypothermia-all activate inflammatory cytokines and oxidative stress. The synergistic impact of systemic proinflammatory mediators activates microglia and promotes neuroinflammation. Acutely, the innate immune response is protective defending against pathogens/toxins; however, when chronic, it causes neuroinflammation and neuronal dysfunction, particularly in brainstem and neocortex. The NTS in the brainstem is an essential multiple signaling hub, and an extremely important central integration site of baroreceptor, chemoreceptor, and a multitude of sensory afferents from gustatory, gastrointestinal, cardiac, pulmonary, and upper airway systems. Owing to persistent neuroinflammation, the dysfunctional NTS exerts deleterious impact on nucleus ambiguus, dorsal motor nucleus of vagus, hypoglossal, parabrachial, locus coeruleus and many key nuclei in the brainstem, and the hippocampus, entorhinal cortex, prefrontal cortex, amygdala, insula, and basal forebrain in the neocortex. The neuronal and synaptic dysfunction emanating from the inflamed NTS may affect its interconnected pathways impacting almost the entire CNS--which is already primed by neuroinflammation, thus promoting cognitive and neuropsychiatric symptoms. The upstream factors discussed here may underpin the neuropathopgenesis of AD. AD pathology is multifactorial; the current perspective underscores the value of attenuating disparate upstream factors--in conjunction with anticholinesterase, anti-inflammatory, immunosuppressive, and anti-oxidant pharmacotherapy. Amelioration of the NTS pathology may be of central importance in countering the neuropathological cascade of AD. The NTS, therefore, may be a potential target of novel therapeutic strategies.

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Cytokine production from peripheral blood mononuclear cells and polymorphonuclear leukocytes in patients studied for suspected obstructive sleep apnea

Cited by 24 publications

References 49 publications

Treatment for sleep apnea by continuous positive airway pressure improves levels of inflammatory markers - a meta-analysis

Treatment for sleep apnea by continuous positive airway pressure improves levels of inflammatory markers - a meta-analysis

Serum Inflammatory Markers in Obstructive Sleep Apnea: A Meta-Analysis

Dysfunctional Nucleus Tractus Solitarius: Its Crucial Role in Promoting Neuropathogentic Cascade of Alzheimer’s Dementia—A Novel Hypothesis

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