Preactivated Peripheral Blood Monocytes in Patients With Essential Hypertension

Dörffel, Yvonne; Lätsch, Christoph; Stuhlmüller, Bruno; Schreiber, Stefan; Scholze, Susann; Burmester, Gerd R.; Scholze, Jürgen

doi:10.1161/01.hyp.34.1.113

Cited by 235 publications

(175 citation statements)

References 30 publications

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“…Our results are somehow different from those previously reported (Table 3). 6,16,21,[33][34][35][36][37] As stated by Hall et al 37 differences in assay methods, population origin and their health status, reagents, sample size, and monocyte numbers might all contribute to the differences observed among studies (Table 3). Our functional study was carried out in healthy homozygous individuals, who had not suffered from infection disease and were free of medication.…”

Section: Discussionmentioning

confidence: 97%

Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases

Correa

Castiblanco

et al. 2004

Genes Immun

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Interleukin-1 beta (IL-1b) exerts a range of inflammatory and immunomodulatory activities that are important in host defense and autoimmune response. The IL-1b gene, located on chromosome 2 (2q13), is polymorphic. The influence of its polymorphism on 355 patients with autoimmune rheumatic diseases was examined. To this effect, 172 patients with rheumatoid arthritis (RA), 114 with systemic lupus erythematosus (SLE), and 69 with primary Sjö gren's syndrome (pSS) were studied. The control group consisted of 392 matched healthy individuals. Genotyping of IL-1b single-nucleotide polymorphisms (SNPs) at positions À511 (C/T) and þ 3953 (C/T) was performed by the polymerase chain reaction-restriction fragment length polymorphism technique. In addition, levels of IL-1b were measured by immunoassay in supernatants of lipopolysaccharide (LPS)-stimulated and nonstimulated peripheral blood monocytes (PBM) obtained from 19 homozygous individuals for the three most common IL-1b likely haplotypes, all belonging to the control group. Allele þ 3953T was protective for SLE (odds ratio (OR) ¼ 0.57, 95% confidence intervals (CI) ¼ 0.34-0.88, P ¼ 0.01) as was the haplotype À511C þ 3953T (OR ¼ 0.43, 95%CI ¼ 0.25-0.74, pc ¼ 0.006). The latter was associated with a lower LPS-stimulated-PBM IL-1b secretion. Results suggest that IL-1b polymorphism influences the susceptibility to acquire SLE in our population. The protective association might be explained by the observed inhibitory effect of IL-1b þ 3953T allele on the secretion of IL-1b under inflammatory circumstances.

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Section: Discussionmentioning

confidence: 97%

Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases

Correa

Castiblanco

et al. 2004

Genes Immun

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“…A clinical study reported that the levels of IL-6 and TNF-α in plasma were correlated with blood pressure in human patients [227]. It also has been shown that hypertension spontaneously activates circulating monocytes and increases reactive oxygen species production in immune cells [228][229][230]. Using leukocyte-specific CCR2-deficient mice, Ishibashi et al [231] revealed the importance of monocyte CCR2 in hypertension.…”

Section: Hypertensionmentioning

confidence: 99%

Microglia and Monocyte-Derived Macrophages in Stroke

2016

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Historically, the brain has been considered an immune-privileged organ separated from the peripheral immune system by the blood-brain barrier. However, immune responses do occur in the brain in neurological conditions in which the integrity of the blood-brain barrier is compromised, exposing the brain to peripheral antigens and endogenous danger signals. While most of the associated pathological processes occur in the central nervous system, it is now clear that peripheral immune cells, especially mononuclear phagocytes, that infiltrate into the injury site play a key role in modulating the progression of primary brain injury development. As inflammation is a necessary and critical component for the subsequent injury resolution process, understanding the contribution of mononuclear phagocytes on the regulation of inflammatory responses may provide novel approaches for potential therapies. Furthermore, predisposed comorbid conditions at the time of stroke cause the alteration of stroke-induced immune and inflammatory responses and subsequently influence stroke outcome. In this review, we summarize a role for microglia and monocytes/macrophages in acute ischemic stroke in the context of normal and metabolically compromised conditions.

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“…Transient transfections in the mouse adrenocortical tumor cell line Y-1 have shown that human renin promoter is responsive to TNF-␣ (5). On the other hand, inflammatory cytokines and particularly TNF-␣, which is an archetypal representative of the cytokine family, seem also to be engaged in blood pressure homeostasis (7,15). Thus TNF-␣ was found to be involved in the control of vascular contraction and proliferation (4,26).…”

mentioning

confidence: 99%

Tumor necrosis factor-α inhibits renin gene expression

Todorov

Müller

Schweda

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Renin, produced in renal juxtaglomerular (JG) cells, is a fundamental regulator of blood pressure. Accumulating evidence suggests that cytokines may directly influence renin production in the JG cells. TNF-α, which is one of the key mediators in immunity and inflammation, is known to participate in the control of vascular proliferation and contraction and hence in the pathogenesis of cardiovascular diseases. Thus TNF-α may exert its effects on the cardiovascular system through modulation of renal renin synthesis. Therefore we have tested the effect of TNF-α on renin transcription in As4.1 cells, which represent transformed mouse JG cells, and in native mouse JG cells in culture. Renin gene expression was also determined in mice lacking the gene for TNF-α (TNF-α knockout mice). TNF-α inhibited renin gene expression via an inhibition of the transcriptional activity, targeting the proximal 4.1 kb of the renin promoter in As4.1 cells. TNF-α also attenuated forskolin-stimulated renin gene expression in primary cultures of mouse JG cells. Mice lacking the TNF-α gene had almost threefold higher basal renal renin mRNA abundance relative to the control strain. The general physiological regulation of renin expression by salt was not disturbed in TNF-α knockout mice. Our data suggest that TNF-α inhibits renin gene transcription at the cellular level and thus may act as a modulator of renin synthesis in (physio)pathological situations.

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Preactivated Peripheral Blood Monocytes in Patients With Essential Hypertension

Cited by 235 publications

References 30 publications

Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases

Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases

Microglia and Monocyte-Derived Macrophages in Stroke

Tumor necrosis factor-α inhibits renin gene expression

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