Association Between Serum Interleukin 10 Level and Development of Heart Failure in Acute Myocardial Infarction Patients Treated by Primary Angioplasty

Rodríguez, Alberto Domínguez; González, Pedro; González, Martín J. García; Hita, Julio Ferrer

doi:10.1016/s1885-5857(06)60248-x

Cited by 6 publications

(4 citation statements)

References 23 publications

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“…In a variety of cell types, IL-10 inhibits the release of proinflammatory mediators [4, 38, 41]. In patients with acute MI, higher serum IL-10 within 24 h after angioplasty is associated with reduced incidence of heart failure progression [9]. After MI, IL-10-deficient mice have increased infarct size and enhanced myocardial necrosis with increased neutrophil infiltration [56].…”

Section: Introductionmentioning

confidence: 99%

IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation

et al. 2017

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Inflammation resolution is important for scar formation following myocardial infarction (MI) and requires the coordinated actions of macrophages and fibroblasts. In this study, we hypothesized that exogenous interleukin-10 (IL-10), an anti-inflammatory cytokine, promotes post-MI repair through actions on these cardiac cell types. To test this hypothesis, C57BL/6J mice (male, 3- to 6-month old, n = 24/group) were treated with saline or IL-10 (50 μg/kg/day) by osmotic mini-pump infusion starting at day (d) 1 post-MI and sacrificed at d7 post-MI. IL-10 infusion doubled plasma IL-10 concentrations by d7 post-MI. Despite similar infarct areas and mortality rates, IL-10 treatment significantly decreased LV dilation (1.6-fold for end-systolic volume and 1.4-fold for end-diastolic volume) and improved ejection fraction 1.8-fold (both p < 0.05). IL-10 treatment attenuated inflammation at d7 post-MI, evidenced by decreased numbers of Mac-3+ macrophages in the infarct (p < 0.05). LV macrophages isolated from d7 post-MI mice treated with IL-10 showed significantly elevated gene expression of M2 markers (Arg1, Ym1, and TGF-β1; all p < 0.05). We further performed RNA-seq analysis on post-MI cardiac macrophages and identified 410 significantly different genes (155 increased, 225 decreased by IL-10 treatment). By functional network analysis grouping, the majority of genes (133 out of 410) were part of the cellular assembly and repair functional group. Of these, hyaluronidase 3 (Hyal3) is the most important feature identified by p value. IL-10 treatment decreased Hyal3 by 28%, which reduced hyaluronan degradation and limited collagen deposition (all p < 0.05). In addition, ex vivo IL-10 treatment increased fibroblast activation (proliferation, migration, and collagen production), an effect that was both directly and indirectly influenced by macrophage M2 polarization. Combined, our results indicate that in vivo infusion of IL-10 post-MI improves the LV microenvironment to dampen inflammation and facilitate cardiac wound healing.

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Section: Introductionmentioning

confidence: 99%

IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation

et al. 2017

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“…Importantly, in patients with severe heart failure the level of serum IL-10 is significantly reduced (Stumpf et al, 2003). Furthermore, survivors of acute myocardial infarction with higher serum IL-10 levels are less likely to develop heart failure (Domínguez Rodríguez et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Signaling via the Interleukin-10 Receptor Attenuates Cardiac Hypertrophy in Mice During Pressure Overload, but not Isoproterenol Infusion

et al. 2020

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Inflammation plays a key role during cardiac hypertrophy and the development of heart failure. Interleukin-10 (IL-10) is a major anti-inflammatory cytokine that is expressed in the heart and may play a crucial role in cardiac remodeling. Based on the evidence that IL-10 potentially reduces pathological hypertrophy, it was hypothesized that signaling via the IL-10 receptor (IL10R) in the heart produces a protective role in reducing cardiac hypertrophy. The aim of this study was to investigate the effects of the ablation of Il-10-r1 gene during pathological cardiac hypertrophy in mice. We found that IL-10R1 gene silencing in cultured cardiomyocytes diminished the anti-hypertrophic effect of Il-10 in TNF-α induced hypertrophy model. We then analyzed mice deficient in the Il-10-r1 gene (IL-10R1 -/mice) and subjected them to transverse aortic constriction or isoproterenol infusion to induce pathological hypertrophy. In response to transverse aortic constriction for 2 weeks, IL-10R1 -/mice displayed a significant increase in the hypertrophic response as indicated by heart weight/body weight ratio, which was accompanied by significant increases in cardiomyocyte surface area and interstitial fibrosis. In contrast, there was no difference in hypertrophic response to isoproterenol infusion (10 days) between the knockout and control groups. Analysis of cardiac function using echocardiography and invasive hemodynamic studies did not show any difference between the WT and IL-10R1 -/groups, most likely due to the short term nature of the models. In conclusion, our data shows that signaling via the IL-10 receptor may produce protective effects against pressure overload-induced hypertrophy but not against β-adrenergic stimuli in the heart. Our data supports previous evidence that signaling modulated by IL-10 and its receptor may become a potential target to control pathological cardiac hypertrophy.

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“…There is also an inflammatory reaction with release of cytokines, growth factors and reactive oxygen species production [26], which contributes to perpetuate ventricular dysfunction and could have important implications for prognosis.…”

Section: Introductionmentioning

confidence: 99%

“…AGE levels are increased in pro-inflammatory and oxidative stress states [26,27]. Either by their direct interaction with proteins, such as extracellular collagen, or by its interaction with its receptor (RAGE), AGE can lead to diastolic, systolic and vascular dysfunction [28].…”

Section: Introductionmentioning

confidence: 99%

Effect of L-Arginine on the Serum Level of Advanced Glycation End Products in Patients with Post Infarction Chronic Heart Failure

Kuryata

Zabida²

2017

J. Nutr. Ther.

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Post-infarction heart failure with preserved ejection fraction (HFpEF) determines a great morbidity and mortality, and given the physiopathology implications of advanced glycation end products (AGEs) in the genesis of myocardial dysfunction. As known endothelial dysfunction is an independent predictor for cardiovascular disease. L-Arginine is the amino acid with potential to improve endothelial function which leading to prevention and treatment of cardiovascular diseases, and we think that L-Arginine may decrease the serum AGEs. We aimed to estimate the value of AGEs in post-infarction HFpEF patients, and detect the effect of L-Arginine on the serum level of AGEs in postinfarction HFpEF pts. all individuals (25) included aged 40 to 80 years, 20(80%) males and 5(20%) females were diagnosed with (HFpEF) according to ESC guidelines (2012), and their functional class according to NYHA classification for HF. 20(80%) patients of them have myocardial infarction in anamnesis. 1 st group:13 patients with HFpEF and history of myocardial infarction with L-Arginine added to their standard treatment. 2 nd group:7 patients with HFpEF and history of myocardial infarction with standard treatment (without L-Arginine). Comparsion group: 5 patients with HFpEF with standard treatment. We prescribed L. Arginine aspartate (Tivortin 4.2gm) intravenously once daily for 10 days for all 1 st group patients. The levels of total cholesterol, triglycerides, glucose, white blood cells, erythrocyte sedimentation rate and AGEs serum level were deterimined. AGEs serum level increased markedly increased in middle-age pts with post infarction HFpEF. Inclusion of L-arginine aspartate in complex of treatment for post infarction HFpEF contributed to the significant decrease AGEs level in >60 years old patients.

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Association Between Serum Interleukin 10 Level and Development of Heart Failure in Acute Myocardial Infarction Patients Treated by Primary Angioplasty

Cited by 6 publications

References 23 publications

IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation

IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation

Signaling via the Interleukin-10 Receptor Attenuates Cardiac Hypertrophy in Mice During Pressure Overload, but not Isoproterenol Infusion

Effect of L-Arginine on the Serum Level of Advanced Glycation End Products in Patients with Post Infarction Chronic Heart Failure

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