Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the cytokine profile of tonsils, cytokine mRNA was determined by reverse transcription-polymerase chain reaction (RT-PCR). The mRNA of interleukin-1 beta (IL 1 beta), IL-2, IL-4, IL-6, IL-8, interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) were expressed on the whole tonsillar tissue of all 5 subjects with recurrent tonsillitis, obstructive sleep apnea syndrome caused by tonsillar hypertrophy or tonsillar focal infection. These cytokine mRNAs were detected in tonsillar mononuclear cells freshly isolated from all or 14 of 15 subjects. The CD4, CD8 and CD19-positive cells were purified using immunomagnetic beads. The CD4-positive cells expressed mRNA of IL-1 beta, IL-2, IL-4, IL-8, IFN-gamma and TNF-alpha. The CD8-positive cells expressed mRNA of IFN-gamma and TNF-alpha. The CD19-positive cells expressed mRNA of IL-1 beta, IL-6, IL-8 and TNF-alpha. Quantitative measurement of PCR products in tonsillar mononuclear cells revealed that the IL-8 mRNA was expressed at a higher level than any other cytokine. A comparison among tonsillar diseases mentioned above revealed that the IL-1 beta and TNF-alpha mRNA were expressed at significantly higher levels in tonsillar mononuclear cells from patients with recurrent tonsillitis than in patients with obstructive sleep apnea syndrome caused by tonsillar hypertrophy. These data indicate that tonsils are active immunologic organs containing a wide variety of cytokines.
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PMID:[A study of cytokine in palatine tonsil--cytokine mRNA expression determined by RT-PCR]. 1019 27

Using two-color flow cytometry, we measured intracellular expression of interleukin-1 alpha (IL-1 alpha), IL-2, IL-4, IL-6, IL-8, interferon gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in tonsillar mononuclear cells freshly isolated and stimulated by phorbol myristate acetate (PMA) and ionomycin. In freshly isolated tonsillar mononuclear cells, IL-1 alpha was produced in 0.39% of CD3 cells, 0.48% of CD4 cells, 0.66% of CD19 and 11.2% of CD14 cells; TNF-alpha was found in 5.4% of CD14 cells. After 8-hour culture without any mitogens, IL-4, IL-8, TNF-alpha and IL-1 alpha were detected in 2.1%, 0.8%, 0.55%, and 0.42% of tonsillar mononuclear cells, respectively. Flow cytometric detection of intracellular cytokines in tonsillar mononuclear cells stimulated with PMA and ionomycin revealed that CD3 cells produced IL-1 alpha, IL-2, IL-4, IL-8, IFN-gamma and TNF-alpha, and CD19 cells produced IL-1 alpha, IL-6, IL-8 and TFN-alpha. In CD3 cells, the number of cells producing IL-2 and TNF-alpha were significantly higher than those expressing other cytokines; and the number of cells producing IFN-gamma and IL-8 were significantly higher than those expressing IL-4 and IL-1 alpha. In CD19 cells, the number of cells producing IL-6 and TNF-alpha were significantly higher than those of IL-8 and IL-1 alpha; and the number of cells producing IL-8 was significantly higher than that of IL-1 alpha. There was no difference in the number of CD3 and CD19 cells producing any cytokine between the adult recurrent tonsillitis group and adult obstructive sleep apnea syndrome group. However, the number of CD3 cells producing IL-2 or TNF-alpha and CD19 cells producing IL-1 alpha, IL-6 or TNF-alpha were significantly lower in children than that of adults (p < 0.05). These findings indicate that the cytokine production in tonsillar mononuclear cells is heterogenous according to the subset and activation and that flow cytometric analysis of intracellular cytokines is a useful means to investigate the pathophysiological role of cytokines in the tonsils.
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PMID:[A study of cytokine in palatine tonsil--flow cytometric analysis of cytokine production in tonsillar mononuclear cells]. 1019 28

About 1.9 % of the population suffer from an obstructive sleep apnea syndrome (OSAS). At the age of between 30 and 60 years it occurs in 3 %. Patients with OSAS develop more frequently such disorders as arteriosclerosis, cardiac arrhythmias and arterial hypertension. A host of pathophysiological changes can be diagnosed. The elevated sympathic activity, recurrent hypoxemias, stress, disturbances in the microvascular milieu, endothelial dysfunction, elevated oxidative capacity as well as a reduced vascular reagibility are deemed to be factors connected to arteriosclerosis. Different biochemical markers, which are seen as risk factors or as markers of cardiovascular diseases, are altered in patients with OSAS (high-sensitive CRP, Interleukin(IL)-6, IL-8, IL-10, TNF-alpha, VGEF, ICAM-1, VCAM-1 and L-Selectin). Patients with OSAS exhibit signs of an impaired insulin sensitivity. Disturbances in microcirculation are also evident. Patients with OSAS have, compared to patients without sleep apnea, elevated blood pressure measurements, even given other common risk factors. The incidence of coronary heart diseases is increased in patients with OSAS. Morbidity and mortality, especially of arteriosclerotic diseases are elevated. Many of the aforementioned disturbances can be improved by a CPAP-therapy.
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PMID:[Cardiovascular diseases and sleep-disordered breathing]. 1525 73

Obstructive sleep apnea (OSA) is a disease with significant morbidity, increased risk of accidents attributed to daytime somnolence, and has been associated with cardiovascular complications. The treatment of choice for OSA is nasal continuous positive airway pressure (nCPAP). Some OSA patients, however, are unable to benefit from this therapy as they find nCPAP intolerable due to the related nasal inflammation. It is hypothesized that nCPAP may cause nasal inflammation in these patients by inducing changes in the expression of genes that encode interleukins (IL-3, IL-4, IL-6, IL-8, IL-13) or adhesion molecules (i.e., ICAM-1) in T-helper lymphocytes. An understanding of the underlying inflammatory mechanism could lead to specific interventions that render nCPAP therapy tolerable for these individuals.
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PMID:Differential gene expression in the T-helper lymphocytes of obstructive sleep apnea patients treated with nasal continuous positive airway pressure (nCPAP). 1532 7

Obstructive sleep apnea (OSA), often concomitant with obesity, increases the risk for the metabolic syndrome. One mechanism that may participate in this association is upregulation of inflammatory pathways. We used structural equation modeling to assess the interrelations between childhood obesity, OSA, inflammation, and metabolic dysfunction. One hundred and eighty-four children (127 boys, mean age: 8.5 +/- 4.1 years) had height and weight measured, underwent overnight polysomnography and had fasting blood taken. The blood was analyzed for insulin, glucose, lipids, leptin, and cytokines [interferon (IFN)-gamma, granulocyte macrophage-colony stimulating factor, interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, tumor necrosis factor-alpha]. Structural equation modeling (SEM) was used to evaluate associations between the outcomes of interest including hypoxia, arousal (related to respiratory and spontaneous), obesity, metabolic dysfunction, and inflammatory markers. Two cytokine factors and one metabolic factor were derived for the SEM. These factors provided good fit in the structural equation model (chi(2)/df = 2.855; comparative fit index = 0.90, root mean squared error of approximation = 0.10) and all factor loadings were significantly different from zero (P < or = 0.01). Overall, our results indicate that while obesity (as measured by body mass index z-score) has a major influence on the metabolic dysfunction associated with OSA, arousal indices, and cytokine markers may also influence this association. Our results support the hypothesis that OSA is a contributor to the mechanisms that link sleep, systemic inflammation and insulin resistance, and show that the interrelations may begin in childhood.
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PMID:Structural equation modeling of sleep apnea, inflammation, and metabolic dysfunction in children. 1803 84

Obstructive sleep apnoea syndrome (OSAS) represents a highly prevalent disease and is recognized as a major public health burden. Large-scale epidemiological studies have demonstrated an independent relationship between OSAS and various cardiovascular disorders. The pathogenesis of cardiovascular complications in OSAS is not completely understood, but given the complexity of the disorder, a multifactorial etiology is likely. Inflammatory processes have emerged as critical in the pathogenesis of atherosclerosis in general and they mediate many of the stages of atheroma formation. Circulating levels of several markers of inflammation have been associated with future cardiovascular risk. These markers include cell adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and selectins, cytokines such as tumour necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6), chemokines such as IL-8, and C-reactive protein (CRP). There is increasing evidence that inflammatory processes also play a central role in the cardiovascular pathophysiology of OSAS. This is supported by cell culture and animal studies identifying a preferential activation of inflammatory pathways by intermittent hypoxia (IH), the hallmark of OSAS. A number of studies have selectively examined the expression of inflammatory factors in OSAS patients with different conclusions. These different findings may have been contributed to by a number of methodological factors such as small subject numbers, inadequately matched study populations, particularly in terms of body mass index (BMI), and inclusion of patients with pre-existing cardiovascular or metabolic diseases. This review will focus on the potential role of various inflammatory markers in OSAS with a critical analysis of the current literature.
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PMID:Inflammatory cardiovascular risk markers in obstructive sleep apnoea syndrome. 1914 46

The pathogenesis of cardiovascular complications in obstructive sleep apnea syndrome (OSAS) is not fully understood but is likely multifactorial in origin. Inflammatory processes play an important role in the pathogenesis of atherosclerosis, and circulating levels of several markers of inflammation have been associated with future cardiovascular risk. These include cell adhesion molecules such as intercellular adhesion molecule-1 and selectins, cytokines such as tumour necrosis factor alpha and interleukin 6, chemokines such as interleukin 8, and C-reactive protein. There is also increasing evidence that inflammatory processes play an important role in the cardiovascular pathophysiology of OSAS and many of the inflammatory markers associated with cardiovascular risk have been reported as elevated in patients with OSAS. Furthermore, animal and cell culture studies have demonstrated preferential activation of inflammatory pathways by intermittent hypoxia, which is an integral feature of OSAS. The precise role of inflammation in the development of cardiovascular disease in OSAS requires further study, particularly the relationship with oxidative stress, metabolic dysfunction, and obesity.
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PMID:Obstructive sleep apnea and inflammation. 1924 45

Obstructive sleep apnoea syndrome (OSAS) is a highly prevalent disease and is recognised as a major public health burden. Large-scale epidemiological studies have demonstrated an independent relationship between OSAS and various cardiovascular disorders. The pathogenesis of cardiovascular complications in OSAS is not completely understood but a multifactorial aetiology is likely. Inflammatory processes have emerged as critical in the pathogenesis of atherosclerosis at all stages of atheroma formation. Increased levels of various circulating markers of inflammation including tumour necrosis factor alpha (TNFalpha), interleukin 6 (IL6), IL-8 and C-reactive protein (CRP) have been reported as associated with future cardiovascular risk. There is increasing evidence of elevated inflammatory markers in OSAS with a significant fall after effective treatment with continuous positive airway pressure. This evidence is particularly strong for TNFalpha, whereas studies on IL6 and CRP have yielded conflicting results possibly due to the confounding effects of obesity. Cell culture and animal studies have significantly contributed to our understanding of the underlying mechanisms of the association between OSAS and inflammation. Intermittent hypoxia, the hallmark of OSAS, results in activation of pro-inflammatory transcription factors such as nuclear factor kappa B (NF-kappaB) and activator protein (AP)-1. These promote activation of various inflammatory cells, particularly lymphocytes and monocytes, with the downstream consequence of expression of pro-inflammatory mediators that may lead to endothelial dysfunction. This review provides a critical analysis of the current evidence for an association between OSAS, inflammation and cardiovascular disease, discusses basic mechanisms that may be responsible for this association and proposes future research possibilities.
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PMID:Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome? 1956 Dec 83

Chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea syndrome represent two of the most prevalent chronic respiratory disorders in clinical practice, and cardiovascular diseases represent a major comorbidity in each disorder. The two disorders coexist (overlap syndrome) in approximately 1% of adults but asymptomatic lower airway obstruction together with sleep-disordered breathing is more prevalent. Although obstructive sleep apnea syndrome has similar prevalence in COPD as the general population, and vice versa, factors such as body mass index and smoking influence relationships. Nocturnal oxygen desaturation develops in COPD, independent of apnea/hypopnea, and is more severe in the overlap syndrome, thus predisposing to pulmonary hypertension. Furthermore, upper airway flow limitation contributes to nocturnal desaturation in COPD without apnea/hypopnea. Evidence of systemic inflammation in COPD and sleep apnea, involving C-reactive protein and IL-6, in addition to nuclear factor-kappaB-dependent pathways involving tumor necrosis factor-alpha and IL-8, provides insight into potential basic interactions between both disorders. Furthermore, oxidative stress develops in each disorder, in addition to activation and/or dysfunction of circulating leukocytes. These findings are clinically relevant because systemic inflammation may contribute to the pathogenesis of cardiovascular diseases and the cell/molecular pathways involved are similar to those identified in COPD and sleep apnea. However, the pathophysiological and clinical significance of systemic inflammation in COPD and sleep apnea is not proven, and thus, studies of patients with the overlap syndrome should provide insight into the mechanisms of systemic inflammation in COPD and sleep apnea, in addition to potential relationships with cardiovascular disease.
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PMID:Chronic obstructive pulmonary disease and obstructive sleep apnea: overlaps in pathophysiology, systemic inflammation, and cardiovascular disease. 1962 78

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 positive correlation was found to occur among IL-8, ICAM-1, and sputum neutrophils, as well as across the apnea-hypopnoea index (AHI), TST 90%, body mass index (BMI), and neck circumference. The data obtained confirm the occurrence of an ICAM- and IL-8-mediated neutrophilic airway inflammation in both OSA and obese patients. The degree of inflammation, which seems to worsen in cases of comorbidity (OSA and obesity), is likely to be responsible for the increased risk of developing cardiovascular events observed in these subjects, and therefore, it deserves to be elucidated even more.
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PMID:Systemic and airway inflammation in sleep apnea and obesity: the role of ICAM-1 and IL-8. 2000 60


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