Interleukin 8 released after acute myocardial infarction is mainly bound to erythrocytes (original) (raw)
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Basic research in cardiology
Polymorphonuclear neutrophils (PMN) are known to participate in the development of tissue injury during myocardial infarction due to both free oxygen radicals release, as well as to their involvement in the "no-reflow" phenomenon. We have previously shown that peripheral blood plasma (obtained from patients with acute myocardial infarction) has chemotactic activity for PMN and is able to induce PMN adherence as well as superoxide anion production. To investigate whether interleukin-8 (IL-8/NAP-1), a potent chemotactic factor for PMN, is involved in plasma-mediated PMN stimulation, we measured plasma levels of IL-8 in five patients with transmural myocardial infarction with highly sensitive enzyme-linked immunosorbent assay (ELISA) using specific antibodies. Blood samples were taken immediately after patients' admission, within 15 and 30 min of treatment with intravenous nitrates, as well as after 1, 2, 3, and 7 days. All samples expressed IL-8 activity within the detec...
Inhibition Of Interleukin-8 Blocks Myocardial Ischemia-Reperfusion Injury
The Journal of Thoracic and Cardiovascular Surgery, 1998
Introduction: Interleukin-8 is thought to play a role in neutrophil activation and transcapillary migration into the interstitium. Because neutrophils are principal effector cells in acute myocardial ischemia-reperfusion injury, we postulated that the inhibition of interleukin-8 activity with a neutralizing monoclonal antibody directed against rabbit interleukin-8 (ARIL8.2) would attenuate the degree of myocardial injury encountered during reperfusion. Methods: In New Zealand White rabbits, the large branch of the marginal coronary artery supplying most of the left ventricle was occluded for 45 minutes, followed by 2 hours of reperfusion. Fifteen minutes before reperfusion, animals were given an intravenous bolus of either 2 mg/kg of ARIL8.2 or 2 mg/kg anti-glycoprotein-120, an isotype control antibody that does not recognize interleukin-8. At the completion of the 120-minute reperfusion period, infarct size was determined. Results: In the area at risk for infarction, 44.3% ؎ 4% of the myocardium was infarcted in the anti-glycoprotein-120 group compared with 24.8% ؎ 9% in the ARIL8.2 group (p < 0.005). In control animals, edema and diffuse infiltration of neutrophils were observed predominantly in the infarct zone and the surrounding area at risk. Tissue myeloperoxidase determinations did not differ significantly between groups, indicating that the cardioprotective effect of ARIL8.2 was independent of an effect on neutrophil infiltration. Conclusions: A specific monoclonal antibody that neutralizes interleukin-8 significantly reduces the degree of necrosis in a rabbit model of myocardial ischemia-reperfusion injury.
PLoS ONE, 2014
Background: No data from controlled trials exists regarding the inflammatory response in patients with de novo heart failure (HF) complicating ST-elevation myocardial infarction (STEMI) and a possible role in the recovery of contractile function. We therefore explored the time course and possible associations between levels of inflammatory markers and recovery of impaired left ventricular function as well as levosimendan treatment in STEMI patients in a substudy of the LEvosimendan in Acute heart Failure following myocardial infarction (LEAF) trial.
Interleukin8 gene induction in the myocardium after ischemia and reperfusion in vivo
Journal of Clinical Investigation, 1995
Neutrophil adhesion and direct cytotoxicity for cardiac myocytes require chemotactic stimulation and are dependent upon CD18-ICAM-1 binding. To characterize the potential role of IL-8 in this interaction, canine IL-8 cDNA was cloned and the mature recombinant protein expressed in Escherichia coli BL21 cells. Recombinant canine IL-8 markedly increased adhesion of neutrophils to isolated canine cardiac myocytes. This adhesion resulted in direct cytotoxicity for cardiac myocytes. Both processes were specifically blocked by antibodies directed against CD18 and IL-8. In vivo, after 1 h of coronary occlusion, IL-8 mRNA was markedly and consistently induced in reperfused segments of myocardium. IL-8 mRNA was not induced in control (normally perfused) myocardial segments. Minimal amounts of IL-8 mRNA were detected after 3 or 4 h of ischemia without reperfusion. Highest levels of induction were evident in the most ischemic myocardial segments. IL-8 mRNA peaked in the first 3 h of reperfusion and persisted at high levels beyond 24 h. IL-8 staining was present in the inflammatory infiltrate near the border between necrotic and viable myocardium, as well as in small veins in the same area. These findings provide the first direct evidence for regulation of IL-8 in ischemic and reperfused canine myocardium and support the hypothesis that IL-8 participates in neutrophil-mediated myocardial injury. (J. Clin. Invest. 1995. 95:89-103.) Methods Molecular cloning. A specific canine IL-8 cDNA probe was initially prepared by reverse transcription-PCR using RNA extracted from lipo-Interleukin-8 in Ischemic and Reperfused Myocardium 89 J. Clin. Invest.
Arquivos brasileiros de cardiologia, 2020
Background Patients with acute myocardial infarction may have a large infarcted area and ventricular dysfunction despite early thrombolysis and revascularization. Objective To investigate the behavior of circulating cytokines in patients with ST-segment elevation myocardial infarction (STEMI) and their relationship with ventricular function. Methods In the BATTLE-AMI (B and T Types of Lymphocytes Evaluation in Acute Myocardial Infarction) trial, patients with STEMI were treated with a pharmacoinvasive strategy. The plasma levels of cytokines (IL-1 β , IL-4, IL-6, IL-10, and IL-18) were tested using enzyme-linked immunosorbent assay (ELISA) at baseline and after 30 days. Infarcted mass and left ventricular ejection fraction (LVEF) were examined by 3-T cardiac magnetic resonance imaging. All p-values < 0.05 were considered statistically significant. Results Compared to baseline, lower levels were detected for IL-1 β (p = 0.028) and IL-18 (p < 0.0001) 30 days after STEMI, whereas...
To evaluate the serum concentrations of proinflammatory cytokines interleukin (IL-1, IL-6, IL-8, IL-18), tumour necrosis factor α (TNF-α), C-reactive protein (CRP), and anti-inflammatory cytokine interleukin 10 (IL-10) regulatory in patients with AMI, and to assess the correlation between anti-inflammatory and pro-inflammatory cytokines in AMI. Thirty patients (13 women and 17 men) with (AMI) enrolled in this study and 30 as control group (10 women and 20 men). There aged varied between 40-60 years old. In this study were measured serum levels of proinflammatory cytokines interleukin (IL-6, IL-1, IL-18, and IL-8), TNF-α, and anti-inflammatory cytokine interleukin 10 (IL-10) in both patient and in control groups by using ELISA technique. Serum levels of interleukine-6, IL-1α, IL-8, and IL-18, CRP, and TNF-α were significantly higher whereas serum IL-10 L level in AMI patients in compares with control group. This study shows a significantly increase in IL-1, IL-18,IL-6,andIL-18 and decrease in IL-10 in the circulation of AMI.
European Heart Journal, 2008
Studies have shown that erythrocyte membranes are present within necrotic cores in atherosclerotic plaques, and that circulating erythrocytes in patients with acute coronary syndrome (ACS) have increased total cholesterol content (CEM). Interleukin-8 (IL-8) binds to erythrocytes and during intraplaque haemorrhage it is released into the plaque and thus may contribute to inflammatory cascade and atherosclerotic plaque instability. The present study was undertaken to test the hypothesis that erythrocyte membrane IL-8 is elevated in patients with ACS compared with those with chronic stable angina (CSA).
Cytokines and adhesion molecules in the course of acute myocardial infarction
Clinica Chimica Acta, 1999
The plasma levels of interleukin 1 beta (IL 1b), interleukin 6 (IL 6), interleukin 8 (IL 8), tumor necrosis factor alpha (TNF-a), E-selectin, ICAM 1 and C-reactive protein (CRP) have been studied in 24 patients with acute myocardial infarction in the course of 96 h. The plasma IL 1b and IL 6 levels were continually elevated during the 96 h study period (the peak of plasma IL 1b level was 22.2 pg / ml, S.D. 8.6, P , 0.001, normal values of IL 1b are less than 10 pg / ml, the mean peak plasma concentration of IL 6 was 184.9 pg / ml, S.D. 134.7, vs. normal values of 15.57 pg / ml, S.D. 2.4, P , 0.001). The mean plasma IL 8 level was increased for the duration of the study, the mean plasma IL 8 level was 103.0 pg / ml, S.D. 23.4 (normal value was below 30 pg / l, S.D. 8.0) P , 0.001. The plasma TNF-a level was elevated throughout the time of observation without any significant peak. The mean plasma TNF-a concentration was 46.8 pg / ml, S.D. 2.13, vs. normal value 4.35 pg / ml, S.D. 1.23, P , 0.001. The plasma E-selectin level reached the mean level of 145.1 ng / ml, S.D. 75.4, vs. normal value 29.1-63.4 ng / ml, P , 0.001 at an interval of 15-42 h after the onset of the symptoms. The plasma ICAM 1 level showed only a slight significant increase during the first 36 h. The plasma CRP concentration increased later than IL 6, and reached a peak at 42 h after the onset of the symptoms (69.2 mg / l, S.D. 29.9, vs. 1.2 mg / l, S.D. 4.7, P , 0.0001). We conclude that cytokines and adhesion molecules can play an important role in the mechanisms of tissue injury in the process of ischemia and reperfusion.
Journal of Cardiovascular Translational Research, 2012
The frequency and function of T cells, monocytes, and dendritic cell subsets were investigated in 12 patients after acute myocardial infarction (AMI)-(T0), 1 month after the episode (T1), and in 12 healthy individuals (HG). The cell characterization and the functional studies were performed by flow cytometry and by RT-PCR, after cell sorting. The most important findings at T0 moment, when compared with T1 and HG, were: a decrease in the frequency of IL-2-producing T cells; a lower frequency of TNF-α-and IL-6-producing monocytes, myeloid dendritic cells, and CD14 −/low CD16 + DCs; and a lower TNF-α mRNA expression, after sorting these cells. Moreover, the regulatory function of Treg cells, at T0 moment, was upregulated, based on the FoxP3, CTLA-4, and TGF-β mRNA expression increase. The majority of these phenotypic and functional alterations disappeared at T1. Our data demonstrate that AMI induces a significant change in the immune system homeostasis.