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Available from: Cornelia M Weyand
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    • "Primary hypertension (PH) is a complex disease consisting of hemodynamic, metabolic, and immune abnormalities. The primary reason for these defects is still unknown, but immune abnormalities are now considered to be the leading factors in the PH pathogenesis [1]. Low-grade systemic inflammation, including innate and adaptive immune response components, seems to play a role in the pathogenesis of PH [2]. "
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    ABSTRACT: The aim of the study was to find out whether peripheral blood leukocyte adiponectin receptors 1 and 2 (AdipoR1, AdipoR2) protein expression patterns (flow cytometry) differ between the primary hypertension children (í µí±› = 57) and healthy controls (í µí±› = 19) and if their expression levels are related to selected clinical parameters. The group of 26 patients [AdipoR(−)] showed lower and the group of 31 patients [AdipoR(+)] showed higher AdipoRs protein expression than the control and each other (í µí±ƒ < 0.01 for neutrophils, í µí±ƒ < 0.05 for monocytes). The AdipoR(+) leukocytes expressed higher AdipoR1 mRNA levels (RT-PCR) than AdipoR(−) ones and controls (í µí±ƒ = 0.022 and í µí±ƒ = 0.007, resp.). Despite greater BMI, the AdipoR(−) patients had unchanged serum adiponectin levels. In contrast, AdipoR(+) patients had lower serum adiponectin concentrations than the AdipoR(−) ones and controls (í µí±ƒ < 0.001). The AdipoR(+) patients had higher blood pressure (í µí±ƒ = 0.042) and greater carotid intima-media thickness (í µí±ƒ = 0.017) than the AdipoR(−) ones. The stage of hypertension was associated with increased neutrophil but not monocyte AdipoR1 density (AdipoR1 MFI) (í µí±ƒ < 0.05). Severe ambulatory hypertension was presented more often in AdipoR(+) patients than in AdipoR(−) ones (51.6% versus 26.9%, resp.; í µí±ƒ < 0.01). In conclusion, neutrophil AdipoRs upregulation was associated with early stages of vascular injury, hypertension severity, and low serum levels of adiponectin.
    Full-text · Article · Feb 2015 · BioMed Research International
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    • "Although the pathogenesis of PE is not fully understood, several works have linked inflammation to cardinal features of this disorder. For instance, preeclamptic placenta secretes several inflammatory molecules as a result of the hypoxic state developed from a lack of vessel remodeling in the uterus [7] [8] [9]. It is well known that regulatory T cells (T regs ) are a particular subset of T lymphocytes (CD4+, CD25 high , Foxp3+) that maintain immunological self-tolerance, suppress the inflammatory state, and induce immune homoeostasis [10] [11]. "
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    ABSTRACT: Regulatory T cells (Tregs; CD4+CD25(high)Foxp3+) are critical in maintaining immune tolerance during pregnancy and uterine vascularization. In this study, we show that, in Mexican women with different preeclamptic severity levels, the number of Tregs and the subset of CD4+CD25(high)Foxp3+ are decreased compared with those of normotensive pregnant women (NP). Moreover, a systemic inflammatory state is a pivotal feature in the pathogenesis of this disorder and could be related to hypertension and endothelial dysfunction. Likewise, we observed elevated levels of IL-6, TNF-α, and IL-8 in the serum of severe preeclamptic patients (SPE); no differences were found in the IL-1β and IL-10 levels compared with those of NP patients. An analysis of chemokines in the preeclamptic serum samples showed high levels of CXCL10, CCL2, and CXCL9. Our findings suggest that the preeclamptic state is linked with systemic inflammation and reduced numbers of Tregs.
    Full-text · Article · Dec 2014 · BioMed Research International
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    • "In the vasculature, activated T cells promote vasoconstriction and remodeling. Together with the promotion of sodium and water retention in the kidney, more severe hypertension can result [61, 62]. "
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    ABSTRACT: Hypertension is a complex condition and is the most common cardiovascular risk factor, contributing to widespread morbidity and mortality. Approximately 90% of hypertension cases are classified as essential hypertension, where the precise cause is unknown. Hypertension is associated with inflammation; however, whether inflammation is a cause or effect of hypertension is not well understood. The purpose of this review is to describe evidence from human and animal studies that inflammation leads to the development of hypertension, as well as the evidence for involvement of oxidative stress and endothelial dysfunction-both thought to be key steps in the development of hypertension. Other potential proinflammatory conditions that contribute to hypertension-such as activation of the sympathetic nervous system, aging, and elevated aldosterone-are also discussed. Finally, we consider the potential benefit of anti-inflammatory drugs and statins for antihypertensive therapy. The evidence reviewed suggests that inflammation can lead to the development of hypertension and that oxidative stress and endothelial dysfunction are involved in the inflammatory cascade. Aging and aldosterone may also both be involved in inflammation and hypertension. Hence, in the absence of serious side effects, anti-inflammatory drugs could potentially be used to treat hypertension in the future.
    Full-text · Article · Jul 2014 · BioMed Research International
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