The relationship between asymptomatic organ damage, and serum soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and Interleukin-17A (IL-17A) levels in non-diabetic hypertensive patients

Abstract

BackgroundThis study aimed to measure the serum soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and interleukin-17A (IL-17A) levels in hypertensive patients with/without asymptomatic organ damage (AOD), as well as to determine the relationship between the serum sTWEAK and IL17-A levels, and carotid intima media thickness (CIMT), proteinuria, retinopathy, and the left ventricle mass index (LVMI).MethodsThe study included 159 patients diagnosed with and followed-up for primary hypertension (HT); 79 of the patients had AOD (61 female and 18 male) and 80 did not (52 female and 28 male). sTWEAK and IL-17A levels were measured in all patients.ResultsThe sTWEAK level was significantly lower in the patients with AOD than in those without AOD (858.4 pg/mL vs. 1151.58 pg/mL, P = 0.001). The sTWEAK level was negatively correlated with the mean microalbuminuria level and LVMI. The median IL-17A level was significantly higher in the patients with AOD than in those without AOD (2.34 pg/mL vs. 1.80 pg/mL, P = 0.001). There was a positive correlation between mean IL-17A level, and mean microalbuminuria level, CIMT, and LVMI. Multivariate logistic regression analysis showed that patient age, sTWEAK level, and mean 24-h systolic blood pressure were predictors of AOD.ConclusionsThe sTWEAK level was lower and IL-17A level was higher in the patients with AOD. It remains unknown if sTWEAK and IL-17A play a role in the pathophysiology of AOD. Prospective observational studies are needed to determine the precise role of sTWEAK and IL-17A in the development of target organ damage.

Interleukin 17A and Toll-like Receptor 4 in Patients with Arterial Hypertension

“…It would appear that although controlled, hypertension can still be a trigger for immune stimulation, as was demonstrated by the close correlation between the duration of controlled hypertension and higher TLR4 expression. On the other hand, the duration of non-controlled hypertension was closely linked to a higher level of IL-17A in serum which is in line with other studies [33, 34] that found association between IL-17A and blood pressure values. Indeed, higher levels of IL-17A might be related to activated innate immunity, could be influenced by the used class of antihypertensive drugs or, as suggested by some authors might have protective role.…”

“…Serum concentrations of IL-17A in our study were low in all patients, which is similar to some other studies [33]. Besides that, it is known that cytokines have short serum half-life and very often undetectable baseline levels.…”

“…It has been shown that this cytokine maintains hypertension and contributes to vascular dysfunction [24]. Higher IL-17A levels are associated with hypertension in patients with diabetes [24] and IL-17 has been closely linked with endothelial dysfunction, hypertension, end stage organ damage, and atherosclerotic conditions [32, 33, 48] exhibiting both pro-inflammatory and protective effect [37]. It was recently reported that shortage of IL-17/IL-23 leads to increased albuminuria and kidney damage in patients with hypertension [52].…”

“…Subsequently, interleukin 17 was discovered to directly increase blood pressure by decreasing endothelial nitric oxide production [32]. In addition, IL-17A level have recently been reported to be higher in non-diabetic patients with hypertension and asymptomatic organ damage compared to those without such damage [33], as well as in a patient population exhibiting prehypertension [34]. It was speculated that IL 17 might have a protective role with respect to cardiovascular diseases [35-37].…”

Rola krążącego sTWEAK w patogenezie choroby Hashimoto — badanie pilotażowe

“…It induces many cellular response and regulates inflammatory pathways depending on the cell type and micro environment [8]. sTWEAK's biological activity may vary by onset period of inflammation.…”