| Background and ObjectivesHeart Failure is the final destination of the majority of cardiovascular disease, is aslo a leading cause of death. In the last decades, we recognized that the neurohormonal mechanism e.g.the excitement of sympathetic nervousor and activation of renin-angiotensin system played an important role in the development of heart failure, this also develop drugs which against these mechanisms, such as:P-blockers, angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB). In recent years, many studies have proved that not only the neurohormonal mechanism, but also a variety of inflammatory cytokines participate in the cardiac and vascular remodeling process during the heart failure. Unlike Thl and Th2, the Th17cells as a new kind of CD4+T cells play a biological role in the regulation of immune response by secreting interleukin-17(IL-17),. The recent studys proved that IL-17is a pro-inflammatory cytokine and its major biological function is related with promoting fibroblast cells to secrete IL-6and inducing NFκB/mitogen activated. Interleukin-35(IL-35) is composed by the subunits of EBI3and IL-12p35which was discovered in2007, It is one of the IL-12family members also a novel anti-inflammatory factor. The IL-35promote the activation of regulatory T cell and inhibit the proliferation of Th17. In this study, we analyzed the relationship between the severity of heart failure and IL-17and IL-35by measuring the concentration of IL-17and IL-35in heart failure patients with different causes, and investigated the probably function of IL-17and IL-35in heart failure patients. Methods:Selected48cases with obvious symptoms of heart failure, including16patients with dilated cardiomyopathy (DCM group),20patients with coronary heart disease, and20patients with hypertensive heart disease. And selected24normal healthy cases as control group. The clinical data of patients that enrolled in our research were recorded, blood samples were drawn when pqtients admitted and7-14days after admission (when the patients condition was stable). The supernatant was put in EP tub after centrifuged, and stored at-80℃. We detected serum levels of IL-17and IL-35of heart failure patients and normal healthy cases by enzyme-linked immunosorbent assay (ELISA). We measured left ventricular end-diastolic diameter (LVEDd, mm), left ventricular end systolic diameter (LVESd, mm) and ejection fraction (EF%) and other data by color Doppler ultrasound.Result:1:The comparison of serum IL-17level in patients with between heart failure group and control group:the serum IL-17level in heart failure patients including acute phase and stable phase was higher than control group, the difference was statistically significant (P<0.01), And in heart failure patients, the serum IL-17levels at acute phase was higher than at stable phase, and the difference was statistically significant (P<0.01).2:The comparison of serum IL-35level in patients with acute between heart failure group and control group the serum IL-35level in heart failure patients including acute phase and stable phase was lower than control group, and the difference was statistically significant (P<0.05). And in heart failure patients, the serum IL-35level at stable phase was higher than acute phase, and the difference had no statistical significance (P>0.05).3:The comparison of serum IL-17level in heart failure patients with different causes, of:In DCM patients, the serum IL-17level at acute phase was higher than stable phase, the difference is statistically significant (P<0.01); In coronary heart disease patients and hypertensive heart disease patients, the difference of serum IL-17level between acute phase and stable phase showed no statistical significance (P>0.05).4:The comparison of serum IL-35levels in heart failure patients with different causes:In DCM patients, the serum IL-35level at acute phase was higher than stable phase, the difference was statistically significant (P<0.01); In coronary heart disease patients and hypertensive heart disease patients, the difference of serum IL-35level between acute phase and stable phase showed no statistical significance (P>0.05).5:The comparison of serum IL-17levels at acute phase in heart failure patients with different causes:The serum IL-17levels in DCM group was significantly higher than CHD and hypertension group (P<0.01), and between CHD and hypertension group the difference had no statistical significance (P>0.05).6:The comparison of serum IL-35level at acute phase in heart failure patients with different causes. At the acute phase, serum IL-35level of DCM group was significantly lower than CHD and hypertension group (P<0.05), and between CHD group and hypertension group the difference had no statistical significance (P>0.05).7:The serum IL-17and IL-35level had a significant negative correlation (r=-0.491, P<0.01).8:Correlation analysis in heart failure patients showed that the level of serum IL-17protein and ventricular ejection fraction (EF) had a negative correlation (r=-0.633, P <0.01), the NYHA class and serum IL-17level was positively correlated (r=0.513, P <0.01).9:Correlation analysis in heart failure patients showed that serum IL-35level and ventricular ejection fraction (EF) had a positively correlation (r=0.530, P<0.01), NYHA class and serum IL-35level was negatively correlated (r=-0.637, P<0.01). Conclusion:1、The serum IL-17level in heart failure patients was significantly increased, and was positively correlated with the degree of heart failure.2、The serum IL-35level of patients with heart failure s was significantly reduced, and negatively correlated IL-35level and degree of heart failure.3、Activation of immune system and inflammation play a role in the development of heart failure. |
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