Opposite Role of Interferon-γ and Interleukin-4 on the Regulation of Blood Pressure in Mice

Heuven-Nolsen, D. van; Kimpe, Sjef J. De; Muis, Thea; Ark, Ingrid van; Savelkoul, H.F.J.; Beems, Rudolf B.; Oosterhout, Antoon J. M. van; Nijkamp, Frans P.

doi:10.1006/bbrc.1998.8742

Cited by 12 publications

(9 citation statements)

References 37 publications

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“…Peng et al found that IL-4 deficiency has no effect on blood pressure values but significantly accelerates cardiac fibrotic remodeling in angiotensin II-induced hypertension [27]. Dicky et al found that anti-IL-4 treatment resulted in a decrease in blood pressure in hypertensive NZBNZWF1 mice, suggesting a role of IL-4 in promoting blood pressure [28]. In contrast, Chatterjee et al found that treatment with exogenous IL-4 significantly decreased blood pressure in P-PIC mice, which is a model of pregnancy-induced hypertension syndrome, indicating a protective role of IL-4 in hypertension [29].…”

Section: Discussionmentioning

confidence: 99%

Circulating Th1, Th2, and Th17 Levels in Hypertensive Patients

Cheng

et al. 2017

Disease Markers

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Background Evidence from experimental studies showed that Th1, Th2, and Th17 play a pivotal role in hypertension and target organ damage. However, whether changes in the circulating Th1, Th2, and Th17 levels are associated with nondipper hypertension and carotid atherosclerotic plaque in hypertension has yet to be investigated. Methods Th1, Th2, and Th17 levels were detected using a flow cytometric analysis, and their related cytokines were measured by enzyme-linked immunosorbent assay in 45 hypertensive patients and 15 normotensive subjects. Results The frequencies of Th1 and Th17 in hypertensive patients, especially in nondipper patients and patients with carotid atherosclerotic plaque, were markedly higher than those in the control group; this was accompanied by higher IFN-γ and IL-17 levels. In contrast, the Th2 frequencies and IL-4 levels in hypertensive patients, especially in nondipper patients and patients with carotid atherosclerotic plaque, were significantly lower than those in the control group. Conclusions The changes in Th1, Th2, and Th17 activity are associated with the onset of the nondipper type and carotid atherosclerotic plaque in hypertensive patients.

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Section: Discussionmentioning

confidence: 99%

Circulating Th1, Th2, and Th17 Levels in Hypertensive Patients

Cheng

et al. 2017

Disease Markers

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“…20 Administration of IFN-␥ to New Zealand white mice has been reported to increase mean arterial pressure. 21 On the other hand, administration of IFN-␥ in Dahl salt-sensitive rats has been shown to reduce blood pressure, 22 while having no effect in spontaneously hypertensive rats. 23 Such variability in the data is consistent with the postulated pathophysiological heterogeneity of hypertension among different experimental models.…”

Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor-α

et al. 2010

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Abstract-In the Sabra rat, oxidative stress (OS) and inflammation precede the development of hypertension. Inhibition of the phagocytic NADPH oxidase attenuates the rise in blood pressure. The present study was set to identify possible priming agents for this enzyme and to test the hypothesis that the phagocytic NADPH oxidase contributes to OS and inflammation. Sabra salt-sensitive and Sabra salt-resistant rats were salt loaded or provided regular chow for 60 days with or without apocynin to inhibit NADPH oxidase. Levels of interleukin 6, tumor necrosis factor-␣, and interferon-␥ served as indices of inflammation. Extracellular and intracellular levels of the polymorphonuclear leukocyte tumor necrosis factor-␣ receptors (p55 and p75) were assessed by flow cytometry in young and adult rats. NADPH oxidase activity and expression of p47phox were measured in polymorphonuclear leukocytes and aortic rings. Malondialdehyde and carbonylated fibrinogen served as indices of OS. Inflammatory and OS indices excluding interferon-␥ were higher in the hypertensive state and reduced by apocynin. Levels of malondialdehyde and tumor necrosis factor-␣ were elevated already in the prehypertensive state. No differences were found in the levels of p75. The extracellular expression of p55 was higher in adult Sabra salt-resistant compared with Sabra salt-sensitive rats (7.46Ϯ2.2% versus 2.1Ϯ0.5%; PϽ0.05), whereas levels of the intracellular p55 were higher in adult Sabra salt-sensitive rats (3.2Ϯ2% versus 1.1Ϯ0.5%; PϽ0.05). In young normotensive rats, the extracellular levels of p55 were higher in Sabra salt-sensitive compared with Sabra salt-resistant rats (10.6Ϯ5.2% versus 2.9Ϯ1.5%; PϽ0.01). Tumor necrosis factor-␣ plays a role in activation of the polymorphonuclear leukocyte NADPH oxidase, thereby contributing to systemic OS, inflammation, and the development of hypertension in this model. We have shown that the polymorphonuclear leukocyte (PMNL) is a significant contributor to OS and inflammation in hypertensive humans and in animal models of hypertension. In pathological disorders associated with atherosclerosis and cardiovascular diseases, such as hypertension, diabetes mellitus, and end-stage renal disease, PMNLs are primed. [7][8][9] In the primed state, PMNLs are more sensitive to local or systemic stimuli because of a previous exposure to a priming agent. Hence, on encountering an additional stimulus, full cell activation occurs, resulting in a robust release of reactive oxygen species and tertiary granule contents into the bloodstream. 10 The primary source for reactive oxygen species in PMNL is the NADPH oxidase, an enzymatic complex, is composed of 3 cytosolic subunits (p40phox, p47phox, and p67phox) and 2 membrane subunits (p22phox and gp91). On cell activation, the cytosolic subunits translocate to the membrane, and the activated enzyme produces superoxide in a process known as the "respiratory burst." 11 We have reported previously that, in the Sabra rat model of hypertension, priming of PMNLs precedes the development o...

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“…In one study, treatment with IL-4 antibodies lowered BP in NZB mice. 46 T H 17 IL-17 is the defining cytokine of T H 17 cells. Several isoforms of IL-17 exist, with IL-17A and -F being the most abundant.…”

Section: T H 1 and T Hmentioning

confidence: 99%

Immune Mechanisms in Arterial Hypertension

Wenzel¹,

Turner²,

Krebs³

et al. 2016

Journal of the American Society of Nephrology

171

148

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Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive endorgan damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.

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Opposite Role of Interferon-γ and Interleukin-4 on the Regulation of Blood Pressure in Mice

Cited by 12 publications

References 37 publications

Circulating Th1, Th2, and Th17 Levels in Hypertensive Patients

Circulating Th1, Th2, and Th17 Levels in Hypertensive Patients

Tumor Necrosis Factor-α

Immune Mechanisms in Arterial Hypertension

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