Evidence for Prohypertensive, Proinflammatory Effect of Interleukin-10 During Chronic High Salt Intake in the Condition of Elevated Angiotensin II Level

Singh, Purnima; Castillo, Alexander; Islam, Mohammed T.; Majid, Dewan S. A.

doi:10.1161/hypertensionaha.117.09401

Cited by 16 publications

(21 citation statements)

References 43 publications

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“…Knockout of IL-12p35, the subunit shared by IL-12 and IL-35, significantly elevated blood pressure in Ang II-infused mice; treatment with IL-12, a proinflammatory cytokine, rather than the anti-inflammatory cytokine IL-35, surprisingly reduced Ang II-induced hypertension in mice [12]. However, the effects of IL-10 on hypertension are still controversial, and both the anti-and the prohypertensive roles have been reported in previous studies [13,14].…”

Section: Introductionmentioning

confidence: 96%

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Yang

Tang

Zhai

et al. 2020

Mediators of Inflammation

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Background. Multiple interleukin (IL) family members were reported to be closely related to hypertension. We aimed to investigate whether IL-9 affects angiotensin II- (Ang II-) induced hypertension in mice. Methods. Mice were treated with Ang II, and IL-9 expression was determined. In addition, effects of IL-9 knockout (KO) on blood pressure were observed in Ang II-infused mice. To determine whether the effects of IL-9 on blood pressure was mediated by the signal transducer and activator of the transcription 3 (STAT3) pathway, Ang II-treated mice were given S31-201. Furthermore, circulating IL-9 levels in patients with hypertension were measured. Results. Ang II treatment increased serum and aortic IL-9 expression in a dose-dependent manner; IL-9 levels were the highest in the second week and continued to remain high into the fourth week after the treatment. IL-9 KO downregulated proinflammatory cytokine expression, whereas it upregulated anti-inflammatory cytokine levels, relieved vascular dysfunction, and decreased blood pressure in Ang II-infused mice. IL-9 also reduced smooth muscle 22α (SM22α) expression and increased osteopontin (OPN) levels both in mice and in vitro. The effects of IL-9 KO on blood pressure and inflammatory response were significantly reduced by S31-201 treatment. Circulating IL-9 levels were significantly increased in patients with the hypertension group than in the control group, and elevated IL-9 levels positively correlated with both systolic blood pressure and diastolic blood pressure in patients with hypertension. Conclusions. IL-9 KO alleviates inflammatory response, prevents phenotypic transformation of smooth muscle, reduces vascular dysfunction, and lowers blood pressure via the STAT3 pathway in Ang II-infused mice. IL-9 might be a novel target for the treatment and prevention of clinical hypertension.

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Section: Introductionmentioning

confidence: 96%

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Yang

Tang

Zhai

et al. 2020

Mediators of Inflammation

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“…Urine volumes were determined from each urine collection, and samples were centrifuged (3,000 rpm/5 min; 4°C) and preserved for determining urinary excretion of sodium and potassium. Urinary excretion of sodium and potassium was assessed by flame photometry (Singh et al, 2013(Singh et al, , 2017.…”

Section: Collection and Analysis Of Urine And Blood Samplesmentioning

confidence: 99%

High‐salt intake reduces renal tissue levels of inflammatory cytokines in mice

et al. 2020

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High salt (HS) intake is usually considered as an aggravating factor to induce inflammatory renal injury. However, the changes in the renal levels of inflammatory cytokines during HS intake is not yet clearly defined. We hypothesize that HS increases renal levels of tumor necrosis factor‐alpha (TNF‐α) and interleukin‐6 (IL‐6) but decreases interleukin‐10 (IL‐10; anti‐inflammatory cytokine) and these responses exacerbate in NO deficient conditions. Both wild‐type (WT) and endothelial NO synthase knockout (eNOSKO) mice (~8 weeks old, n = 6 in each group) were given normal‐salt (NS; 0.3% NaCl) and HS (4% NaCl) containing diets for 2 weeks. Systolic blood pressure (SBP) was determined by tail‐cuff plethysmography and urine collections were made using metabolic cages. Basal SBP was higher in eNOSKO than WT mice (131 ± 7 vs 117 ± 3 mmHg; p < .05). HS intake for 2 weeks increased SBP in eNOSKO (161 ± 5 mmHg) but not in WT mice. In NS groups, the cytokine levels in renal tissues (measured using ELISA kits and expressed in pg/mg protein) were significantly higher in eNOSKO than WT mice (TNF‐α, 624 ± 67 vs. 325 ± 73; IL‐6, 619 ± 106 vs. 166 ± 61; IL‐10, 6,087 ± 567 vs. 3,929 ± 378). Interestingly, these cytokine levels in HS groups were significantly less both in WT (TNF‐α, 114 ± 17; IL‐6, 81 ± 14; IL‐10, 865 ± 130) and eNOSKO (TNF‐α, 115 ± 18; IL‐6, 56 ± 7; IL‐10, 882 ± 141) mice. These findings indicate that HS induces downregulation of cytokines in the kidney. Such HS‐induced reduction in cytokines, particularly TNF‐α (a natriuretic agent), would facilitate more salt‐retention, and thus, leading to salt‐sensitive hypertension in NO deficient conditions.

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“…21,22 These results suggest that the use of compounding CDs, such as β-CD, Moreover, anti-inflammatory cytokines can effectively decrease the generation of the pro-inflammatory cytokines. 54 IL-10 is a potent anti-inflammatory cytokine and reduces pro-inflammatory cytokines production, including IL-1β, TNF-α, and IL-6 55 . In addition, endogenous and exogenous IL-10 counteracts vascular dysfunction and activity of angiotensin II in hypertensive mice, partially through the modulation of the RhoA-Rho kinase pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, oxidative stress and endothelial dysfunction are involved in the inflammatory cascade that contribute to alterations of the immune response, as well as an increase in adhesion molecule expression, immune cell activation and infiltration, cytokine release and oxidative stress formation. Various pro-inflammatory cytokines, such as tumour necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-18 induce inflammation and otherpro-hypertensive effects, contribute to the increased contractile activity and total peripheral vascular resistance, which directly affect blood pressure [51][52][53][54]. Considering the important role of IL-1β during the inflammatory response in hypertension, we evaluated the effect of CARV and CARV/β-CD treatment on inflammatory cytokine levels.…”

mentioning

confidence: 99%

Antihypertensive effect of carvacrol is improved after incorporation in β‐cyclodextrin as a drug delivery system

Silva

Camargo

Moraes

et al. 2020

Clin Exp Pharma Physio

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Hypertension is a major public health concern globally and a risk factor for cardiovascular diseases (CVD). 1 The number of hypertensive adults increased from 594 million in 1975 to 1.13 billion in 2015, mainly in low-income and middle-income countries. 2 Moreover, in Brazil, approximately one quarter of the adult population are reported to have hypertension. 3 Globally, CVD was responsible for approximately 17.5 million deaths in 2012. If current trends continue, the annual number of deaths will increase to 22.2 million by 2030. 4 Frequently, hypertension is associated with metabolic disorders, functional or structural alterations of target organs, which are aggravated by behavioural risk factors, such as smoking, obesity, excessive salt intake and aging. The most common form of hypertension is "essential hypertension"; however, the causes remain unknown. 5,6 The treatment of hypertension includes some classes of drugs, including: beta-blockers, diuretics, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, calcium channel

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Evidence for Prohypertensive, Proinflammatory Effect of Interleukin-10 During Chronic High Salt Intake in the Condition of Elevated Angiotensin II Level

Cited by 16 publications

References 43 publications

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

High‐salt intake reduces renal tissue levels of inflammatory cytokines in mice

Antihypertensive effect of carvacrol is improved after incorporation in β‐cyclodextrin as a drug delivery system

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