Increased 8-Isoprostane and Interleukin-6 in Breath Condensate of Obstructive Sleep Apnea Patients

Carpagnano, Giovanna Elisiana; Kharitonov, Sergei A.; Resta, Onofrio; Gramiccioni, E; Barnes, Peter J.

doi:10.1378/chest.122.4.1162

Cited by 245 publications

(183 citation statements)

References 17 publications

Supporting

Mentioning

153

Contrasting

Unclassified

Order By: Relevance

“…Obesity is one of the strongest risk factors for developing OSAS (3,4). Meanwhile, clinical and fundamental studies suggest that inflammation involves the pathogenesis of OSAS (5)(6)(7)26,27) and IL-6 was reported to phenotypically increase in patients with OSAS (28)(29)(30). In an attempt to elucidate the relationship between genetic variants in the IL-6 gene and OSAS, we provided two aspects of support with a population-based study.…”

Section: Discussionmentioning

confidence: 91%

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Zhang

Liu²,

Li³

et al. 2009

Int J Mol Med

View full text Add to dashboard Cite

Abstract. Obesity and inflammation are known to correlate with the pathogenesis of obstructive sleep apnea syndrome (OSAS). Interleukin (IL)-6, an important regulator of obesity and inflammation, was reported to phenotypically increase in patients with OSAS. This study aimed to investigate whether genetic variants in IL-6 confer susceptibility to OSAS. The study population consisted of 151 patients with OSAS and 75 healthy controls from Southeast China. Five haplotype-tagging single nucleotide polymorphisms (tSNPs) were selected across 21 kb of the IL-6 locus using Haploview software V4.1. The tSNPs were amplified by polymerase chain reaction (PCR) and genotyped by restriction enzyme digestion followed by gel electrophoresis. Linkage disequilibrium (LD) and haplotype reconstruction were carried out by means of a SHEsis program. No distribution difference of any of the five tSNPs between OSAS patients and controls was observed. However, in nonobese individuals (n=117), the minor allele G (rs1800796) decreased risk of OSAS compared with the major allele C [odds ratio (OR), 0.48; 95% confidence interval (CI), 0.26-0.86; p=0.014], and the haplotype TG (rs1880242, rs1800796) conferred a significantly decreased risk of OSAS than single allele G (rs1800796) (OR, 0.39; 95% CI, p=0.003). Moreover, the severity of sleep-disordered breathing (measured by apnea hypopnea index) increased linearly in carriers of the C variant of IL-6 -572G/C polymorphism (14.3±5.1, 22.0±3.6 and 34.8±3.5 for GG, CG and CC, respectively; p=0.012). To the best of our knowledge, this is the first study to suggest that genetic variants in IL-6 could modify OSAS susceptibility. SNP genotyping of IL-6 is a potential strategy for detecting the risk of breathing disordered diseases in non-obese individuals.

show abstract

Section: Discussionmentioning

confidence: 91%

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Zhang

Liu²,

Li³

et al. 2009

Int J Mol Med

View full text Add to dashboard Cite

show abstract

“…17) Several recent studies have indicated that CRP and proinflammatory cytokines such as IL-6 were elevated in OSAS as well as obesity. [13][14][15]18,19) Thus, obesity and OSAS are inflammatory states, as evidenced by elevated levels of serum markers of systemic inflammation.…”

Section: Discussionmentioning

confidence: 99%

<b>Elevated C-Reactive Protein Levels and Increased Cardiovascular Risk in Patients With Obstructive Sleep Apnea Syndrome</b>

et al. 2005

View full text Add to dashboard Cite

SUMMARYObstructive sleep apnea syndrome (OSAS) is associated with cardiovascular morbidity and mortality. Inflammatory processes associated with OSAS may contribute to cardiovascular morbidity in these patients. C-reactive protein (CRP) is an important serum marker of inflammation. We tested the hypothesis that patients with OSAS have increased plasma CRP.After 173 male subjects underwent polysomnography, 94 were considered to have OSAS (apnea-hypopnea index (AHI) > 5), 38 cardiovascular disease (CVD), and 56 without CVD. Seventy-nine subjects were considered not to have OSAS (AHI < 5) and from among these 57 patients without CVD were enrolled as control subjects.Serum CRP levels were significantly elevated in the OSAS + CVD group compared to the two other groups (P < 0.05). When we evaluated the association between the serum CRP level and severity of OSAS, CRP levels were positively correlated with AHI in OSAS patients (r = 0.61, P < 0.001) OSAS, as a marker of inflammation and cardiovascular risk, is associated with elevated levels of CRP. According to these results, the link between cardiovascular morbidity and OSAS may be explained by the coexistence of other cardiovascular risk factors such as circulating CRP levels. (Int Heart J 2005; 46: 801-809) Key words: CRP, Sleep apnea, Inflammation OBSTRUCTIVE sleep apnea syndrome (OSAS) is a common disorder that affects both children and adults. It is characterized by periods of breathing cessation (apnea) and periods of reduced breathing (hypopnea). Both types of events have similar pathophysiology and are generally considered to be equal with respect to their impact on patients. There are several methods of quantifying the severity of the disorder such as measuring the number of apneas and hypopneas per hour of sleep (the apnea-hypopnea index: AHI), the severity of oxygen desatFrom the

show abstract

“…An increasing body evidence supports the existence of local and systemic inflammation in the upper airway of both adults and children afflicted with OSA (30,31). Indeed, increased levels of NO, IL-6, and 8-isopentane can be detected in exhaled condensates from the upper airway of adults with OSA (32)(33)(34), and increased numbers of neutrophils, as well as increased concentrations of bradykinin and vasointestinal peptide have been measured in nasal lavage fluid from such patients (35). Furthermore, adenotonsillar tissues of children with OSA display increased expression levels of leukotriene receptors along with increased concentrations of leukotrienes (36,37).…”

Section: Discussionmentioning

confidence: 99%

Neurotrophins and Tonsillar Hypertrophy in Children With Obstructive Sleep Apnea

et al. 2007

View full text Add to dashboard Cite

Enlarged adenotonsillar tissue (AT) is a major determinant of obstructive sleep apnea (OSA) severity in children; however, mechanisms of AT proliferation are poorly understood. We hypothesized that early exposure to respiratory syncytial virus (RSV) may modify AT proliferation through up-regulation of nerve growth factor (NGF)-neurokinin 1 (NK1) receptor dependent pathways. AT harvested from 34 children with OSA and 25 children with recurrent tonsillitis (RI) were examined for mRNA expression of multiple growth factors and their receptors. In addition, NK1 receptor expression and location, and substance P tissue concentrations were compared in AT from OSA and RI children. NGF mRNA and its high-affinity tyrosine kinase receptor (trkA) expression were selectively increased in OSA (p Ͻ 0.001). NK1 receptor mRNA and protein expression were also enhanced in OSA (p Ͻ 0.01), and substance P concentrations in OSA patients were higher than in RI (p Ͻ 0.0001). AT from OSA children exhibit distinct differences in the expression of NGF and trkA receptors, NK1 receptors, and substance P. The homology between these changes and those observed in the lower airways following RSV infection suggests that RSV may have induced neuro-immunomodulatory changes within AT, predisposing them to increased proliferation, and ultimately contribute to emergence of OSA. O bstructive sleep apnea syndrome (OSA) is a common and highly prevalent disorder in the pediatric age range, affecting 2-3% of all children (1). Adenotonsillar hypertrophy is by far the major pathophysiological contributor to OSA in children (2,3), and adenotonsillectomy (T&A) currently remains the first line of treatment for children with OSA (4). If left untreated, OSA can result in serious morbid consequences that affect neurocognitive, behavioral and cardiovascular systems (5-9). However, the mechanisms underlying the regulation of benign follicular lymphoid proliferation and hyperplasia are so far extremely poorly understood, such that prediction of which children will develop adenotonsillar hypertrophy is impossible at this stage. It has now been recognized by several epidemiologic studies that factors such as environmental smoking, allergies, and intercurrent respiratory infections are all associated with either transient or persistent hypertrophy of lymphadenoid tissue in the upper airways of snoring children (10 -12). Interestingly, all of these risk factors involve the generation of an inflammatory response, suggesting that the latter may promote the onset and maintenance of proliferative signals to lymphadenoid tissues.Bronchial-associated lymphoid tissue in the lungs of RSVinfected rats express high levels of the neurokinin 1 (NK1) receptor for substance P that is released from subepithelial sensory nerve fibers, a part of the nonadrenergic noncholinergic system (13,14). Furthermore, nerve growth factor (NGF), a major controller of sensorineural development and immuno-inflammatory responses, and its tyrosine kinase A receptor (trkA) are both overexpressed...

show abstract

Increased 8-Isoprostane and Interleukin-6 in Breath Condensate of Obstructive Sleep Apnea Patients

Cited by 245 publications

References 17 publications

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

Genetic variants in interleukin-6 modified risk of obstructive sleep apnea syndrome

<b>Elevated C-Reactive Protein Levels and Increased Cardiovascular Risk in Patients With Obstructive Sleep Apnea Syndrome</b>

Neurotrophins and Tonsillar Hypertrophy in Children With Obstructive Sleep Apnea

Contact Info

Product

Resources

About