The concentration of tumor necrosis factor in the blood serum and in the urine and selected early organ damages in patients with primary systemic arterial hypertension

Puszkarska, Anna; Niklas, Arkadiusz; Głuszek, Jerzy; Lipski, Dawid; Niklas, Karolina

doi:10.1097/md.0000000000015773

Cited by 20 publications

(13 citation statements)

References 48 publications

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“…Nonetheless, based on available literature regarding patients with hypertension without CSC, we may speculate that cytokines that were shown to be elevated in our study are also elevated in the general population of patients with hypertension. The cytokines IL‐6 (Zhang et al 2012), IL‐8 (Marek‐Trzonkowska et al 2015) and TNF‐α (Puszkarska et al 2019) are considered to play an important role in the pathogenesis of hypertension, but their excessive levels were also reported to negatively affect the function of numerous organs. Chae et al (2001) reported increased blood pressure as a stimulus for inflammatory response and hypothesized this to be a mechanism underlying the role of hypertension as a risk factor for atherosclerotic disease.…”

Section: Discussionmentioning

confidence: 99%

Altered plasma cytokine levels in acute and chronic central serous chorioretinopathy

Karska‐Basta

Pociej‐Marciak

Chrząszcz

et al. 2020

Acta Ophthalmologica

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Purpose To evaluate plasma levels of selected cytokines and investigate their correlation with choroidal thickness (CT) in patients with acute and chronic central serous chorioretinopathy (CSC). Methods We enrolled 30 patients with acute CSC, 30 patients with chronic CSC and 20 controls. Plasma concentrations of 12 cytokines, interleukins IL‐8, IL‐1β, IL‐2, IL‐4, IL‐5, IL‐6, IL‐10 and IL‐12 p70, granulocyte‐macrophage colony‐stimulating factor, interferon‐γ, tumour necrosis factor‐α (TNF‐α) and vascular endothelial growth factor (VEGF), were measured using multiplex immunoassays. Differences in cytokine levels between groups were assessed. We also investigated correlations between cytokine levels and CT using swept‐source optical coherence tomography, as well as an association between plasma cytokine profile and systemic hypertension. Results We noted differences in IL‐6 (p = 0.005), IL‐10 (p = 0.03), IL‐12 p70 (p = 0.028) and VEGF (p = 0.029) levels between groups. Pro‐inflammatory IL‐12 p70 and multidirectional IL‐10 cytokines were upregulated, while pro‐angiogenic VEGF was downregulated in chronic CSC as compared with controls (p = 0.005, p = 0.025 and p = 0.027, respectively). Interleukin‐6 (IL‐6) was upregulated in acute and chronic CSC (p = 0.030 and p = 0.005, respectively). Interleukin‐5 (IL‐5), IL‐6 and IL‐12 levels correlated with mean CT in acute CSC (p = 0.008, p = 0.003 and p = 0.044, respectively), while IL‐8, IL‐6 and TNF‐α plasma levels correlated with hypertension in chronic CSC (p = 0.005, p = 0.033 and p = 0.001, respectively). Conclusion We provided new evidence for the possible role of plasma cytokines in the pathogenesis of CSC. Our results suggest that IL‐6 may be important in the pathophysiology of acute and chronic CSC. The association between inflammatory response and hypertension in patients with CSC was also confirmed.

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Section: Discussionmentioning

confidence: 99%

Altered plasma cytokine levels in acute and chronic central serous chorioretinopathy

Karska‐Basta

Pociej‐Marciak

Chrząszcz

et al. 2020

Acta Ophthalmologica

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“…Thus, cytokines may play an important role in modulating excitatory signaling pathways in the hypothalamus contributing to AngII-mediated hypertension. In particular, the proinflammatory mediator tumor necrosis factor a (TNFa) has been implicated in autonomic processes, including the development of hypertension in species as diverse as mice (Sriramula et al, 2008) and humans (Puszkarska et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor α Receptor Type 1 Activation in the Hypothalamic Paraventricular Nucleus Contributes to Glutamate Signaling and Angiotensin II-Dependent Hypertension

et al. 2020

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There are significant neurogenic and inflammatory influences on blood pressure, yet the role played by each of these processes in the development of hypertension is unclear. Tumor necrosis factor a (TNFa) has emerged as a critical modulator of blood pressure and neural plasticity; however, the mechanism by which TNFa signaling contributes to the development of hypertension is uncertain. We present evidence that following angiotensin II (AngII) infusion the TNFa type 1 receptor (TNFR1) plays a key role in heightened glutamate signaling in the hypothalamic paraventricular nucleus (PVN), a key central coordinator of blood pressure control. Fourteen day administration of a slow-pressor dose of AngII in male mice was associated with transcriptional and post-transcriptional (increased plasma membrane affiliation) regulation of TNFR1 in the PVN. Further, TNFR1 was shown to be critical for elevated NMDA-mediated excitatory currents in sympathoexcitatory PVN neurons following AngII infusion. Finally, silencing PVN TNFR1 prevented the increase in systolic blood pressure induced by AngII. These findings indicate that TNFR1 modulates a cellular pathway involving an increase in NMDA-mediated currents in the PVN following AngII infusion, suggesting a mechanism whereby TNFR1 activation contributes to hypertension via heightened hypothalamic glutamate-dependent signaling.

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“…[ 31 ] IL-5, IL-6, and IL-12 levels correlated with mean choroidal thickness in aCSC while IL-6, IL-8, and tumor necrosis factor-alpha plasma levels correlated with hypertension in cCSC. [ 31 56 57 ] IL-6 and VEGF alter the junctional integrity of RPE and downregulate occludin and zonula occludens-1. Therefore, the authors speculated that increased levels of pro-inflammatory cytokines could lead to abnormal endothelium-dependent vasodilation, increased vascular permeability, and angiogenesis, which all have been found to be characteristic of CSC.…”

Section: Immune Mechanisms In Central Serous Chorioretinopathymentioning

confidence: 99%

Central serous chorioretinopathy

Jain¹,

Mohan

Dijk

2022

Taiwan Journal of Ophthalmology

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Central serous chorioretinopathy (CSC) has remained an enigmatic disease since its initial description by Von Graefe. Over the years, multiple risk factors have been recognized: these include psychological stress, behavioral traits, and corticosteroids. The basic pathophysiology of CSC involves choroidal thickening, vascular congestion, altered choroidal blood flow (ChBF), and choroidal hyperpermeability, leading to retinal pigment epithelium decompensation and subsequent neurosensory detachment. Multiple organ systems, mainly the nervous, cardiovascular, endocrinal, and renal systems participate in the control of the vascular tone and the ChBF via hypothalamus–pituitary–adrenal axis and renin–angiotensin–aldosterone system, while others such as the hepatic system regulate the enzymatic degradation of corticosteroids. Many vasoactive and psychotropic drugs also modulate the ocular perfusion. In addition, there are anatomical and genetic predispositions that determine its progression to the chronic or recurrent form, through cellular response and angiogenesis. We herein review the basic pathophysiology and immunogenetics in CSC along with the role of multiple organ systems. With this background, we propose an etiological classification that should provide a framework for customized therapeutic interventions.

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The concentration of tumor necrosis factor in the blood serum and in the urine and selected early organ damages in patients with primary systemic arterial hypertension

Cited by 20 publications

References 48 publications

Altered plasma cytokine levels in acute and chronic central serous chorioretinopathy

Altered plasma cytokine levels in acute and chronic central serous chorioretinopathy

Tumor Necrosis Factor α Receptor Type 1 Activation in the Hypothalamic Paraventricular Nucleus Contributes to Glutamate Signaling and Angiotensin II-Dependent Hypertension

Central serous chorioretinopathy

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