In particular, IL6 levels were significantly higher (p = 0.013) in severe OSA patients (apnea/hypopnea index >30) and were inversely correlated with both mDC2 (r = -0.802, p < 0.007) and pDC (r = -0.317, p = 0.04) subsets.
We found VWF rs1063856 (OR = 1.50, 95% CIs = 1.10-2.04; p = 0.010), IL-6rs1800796 (OR = 1.32, 95% CIs = 1.11-1.56; p = 0.002), TNF rs1800629 (OR = 1.44, 95% CIs = 1.13-1.83; p = 0.003), and CRP rs2794521 (OR = 1.27, 95% CIs = 1.04-1.55; p = 0.021) were all significantly associated with increased susceptibility of OSA, while VWF rs1063856 (OR = 1.75, 95% CIs = 1.18-2.62; p = 0.006), IL-6rs1800796 (OR = 1.39, 95% CIs = 1.10-1.76; p = 0.006) were associated with the severity of OSA.
Here we evaluate oxidative stress markers (TBARS, AOPP, SOD), proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8), anti-inflammatory cytokines (IL-4, IL-10), and cell-free DNA levels before and after 8-week CPAP treatment or moderate-intensity aerobic training in moderate to severe OSA.
Serum levels of leptin, macrophage migration inhibitory factor (MIF), interleukin-6 (IL-6), high sensitive C-reactive protein (Hs-CRP), and tumor necrosis factor alpha (TNF-α) were significantly higher, and adiponectin levels were significantly lower in OSA with NAFLD subjects.
Here, the published links between OSAS and systemic inflammation will be critically reviewed, with special focus on the pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), since these constitute classical prototypes of the large spectrum of inflammatory molecules that have been explored in OSAS patients.
Compared to the 17 children without OSA, those with OSA had higher resting serum IL-6 levels compared to those without (median 3.22 pg/ml vs. 2.31, p < 0.05).
The C, T and R alleles of IL-6, CRP and LEPR genes was more frequent in OSA and NAFLD subjects and significantly correlated with higher protein levels.
Plasma biomarkers of systemic inflammation were significantly increased in patients with moderate OSA (interleukin [IL]-6 and tumor necrosis factor alpha [TNF-α]) and severe OSA (IL-6, TNF-α, high-sensitivity C-reactive protein) when compared with controls (<i>P</i> < .001).
Current advances suggest IL-6 may be important in regulating the sleep-wake cycle, and serum soluble IL-6 receptor (sIL-6R) levels may reflect the severity of OSA.
Total tau and IL-6 concentrations were elevated in participants with moderate-severe OSA, with a mean apnea-hypopnea index (AHI) of 26.1/h, compared to those with mild OSA (mean AHI 8.6/h) and healthy controls (mean AHI 2.1/h).
The group with both asthma and OSA had higher CRP, higher IL-6, a longer sleeping time in stage N1 sleep and stage N2 sleep, and less time in stage R sleep than the control group with no asthma or OSA.
Fasting plasma concentrations of IL-6, hepcidin, and sTfR were measured and evaluated according to glycemic status (T2DM/IGT and normal glucose tolerance) and the presence of OSA.
Metabolic equivalent was negatively associated to cardiometabolic markers, such as C-reactive protein (exp(<i>B</i>)=0.720; p=0.001), interleukin-6 (exp(<i>B</i>)=0.991; p=0.03), insulin (exp(<i>B</i>)=0.982; p=0.03), triglycerides (exp(<i>B</i>)=0.997; p<0.001), homeostasis model assessment for insulin resistance (exp(<i>B</i>)≤0.946; p<0.024), quantitative insulin sensitivity check index (exp(<i>B</i>)=992.4; p<0.001) and mean arterial pressure (exp(<i>B</i>)=0.987; p=0.001).Physical activity was a protective factor against type 2 diabetes mellitus in apnoeic individuals; moreover, being active reduced the risk of developing OSA and was associated with a better cardiometabolic profile.
Serum IL-1β was also slightly higher in nonobese OSA males, but with statistical significance, than in nonobese (19.39 ± 4.67 ng/L vs 17.25 ± 3.66 ng/L, P = .041), and obese non-OSA ones (19.39 ± 4.67 ng/L vs 17.42 ± 3.79 ng/L, P = .047), whereas other biomarkers, IL-6 and TNF-a did not show significant differences among groups.
Resting AT blood flow was higher in OSAS compared to controls (108.5±22.7 vs. 78.9±24.9au, P<0.005) and strongly associated with inflammation markers IL-6 and MCP-1.
The levels of IL-1β as well as IL-6 showed a potential increase, while the levels of IFN-γ (p<0.05; power>0.8) and the ratio IFN-γ/IL-4 in the blood were possibly decreased in OSA.
Objective EDS (lower MSLT) in OSA patients was associated with significantly elevated 24-hour (β = -0.34, p = .01), daytime (β = -0.30, p = .02) and nighttime (β = -0.38, p < .01) IL-6 levels, and significantly decreased daytime (β = 0.35, p = .01) cortisol levels.
OSA increased serum levels of C-reactive protein and 8-isoprostane and elevated the expression of malondialdehyde, tumor necrosis factor α, interleukin (IL)-1β and IL-6 in the pulmonary tissue.
The goal of this study was to assess the association of PVT with objectively measured sleepiness (MSLT) and subjectively measured sleepiness (ESS) and IL-6 levels in patients with OSA.
We hypothesized that the effects of TNF-α in OSAHS might be due to linkage disequilibrium of the TNF-α (-308A) single nucleotide polymorphism (SNP) with other polymorphisms within the TNF-α gene, and that predisposition to elevated IL-6 and IL-8 levels in OSAHS might be attributable to pro-inflammatory IL-6 and IL-8 gene promoter polymorphisms.
Genetic variation in the IL-6/CRP pathway was associated with increased risk for OSA in European American children and may account for the higher CRP levels in the context of pediatric OSA compared to Greek children.