Induction of Cytokine Expression in Leukocytes in Acute Myocardial Infarction

Marx, Nikolaus; Neumann, Franz‐Josef; Ott, Ilka; Gawaz, Meinrad; Koch, Werner; Pinkau, Tobias; Schömig, Albert

doi:10.1016/s0735-1097(97)00116-2

Cited by 124 publications

(60 citation statements)

References 31 publications

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“…Interleukin-6 seemed to be an important cytokine produced by the injured myocytes in a study of 15 patients with AMI (11), and strong negative correlation between serum IL-6 concentration and left ventricular ejection fraction (LVEF) has been demonstrated (12). Similar observations have been made by studying tumor necrosis factor-a (TNF-a), IL-1a and soluble IL-2 receptor (sIL-2-R) which were found to be significantly elevated in AMI, with the highest levels noted in the most severe and complicated cases of myocardial infarction (9,13).…”

Section: Introductionmentioning

confidence: 71%

“…On the other hand, the association between serum levels of cytokines and myocardial ischemia and injury is under investigation. It is known from several studies that several cytokines can be found elevated in patients with cardiac ischemia or AMI (7)(8)(9). From in vitro studies it is of particular interest that ischemic myocytes produce cytokines such as interleukin-6 (IL-6) and its synthesis is accelerated by reperfusion (10).…”

Section: Introductionmentioning

confidence: 99%

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The role of cytokines and cortisol in the non-thyroidal illness syndrome following acute myocardial infarction

Karga

Papaioannou

Venetsanou

et al. 2000

European Journal of Endocrinology

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Objective: A number of different hormone changes have been described during the acute myocardial infarction (AMI), including those of the non-thyroidal illness syndrome (NTIS). Design and methods:We assessed the alterations of serum thyroid hormones, cytokines and cortisol levels in 30 patients with a first episode of AMI 4, 24, 48 h and 10 days (240 h) after the onset of the chest pain and we investigated the possible relationship of these alterations with the severity of AMI. Results: Fifteen patients had left ventricular ejection fraction (LVEF) Յ 50% (group I) and 15 patients had LVEF > 50% (group II). A transient decrease of total tri-iodothyronine (T 3 ), more prominent in group I (P < 0.05, t-test) with a concomitant rise of reverse T 3 (rT 3 ) occurred at 24 h. Total thyroxine (T 4 ), free T 4 (FT 4 ) and free T 4 index did not change significantly, but tended to be higher in group I patients, whereas TSH significantly increased in group II at 48 h. Interleukin-6 (IL-6) increased significantly at 24 h only in group I and declined thereafter (24 vs 240 h, P < 0.001) and this temporal change of IL-6 was associated with similar changes of creatine phosphokinase and creatine kinase isoenzyme MB (CK-MB). Tumor necrosis factor-a and IL-1b remained low in both groups. Cortisol was higher at 4 h and in 12 patients was above the normal values. Negative correlation was found between LVEF and IL-6 (P < 0.001), whereas T 3 , T 4 or cortisol levels were not correlated with the LVEF. Conclusions: Our data indicate that NTIS, in association with increase of IL-6, occurs in the early postinfarction period. In the NTIS following AMI the high level of IL-6 is the best predictor, among several parameters, of the severity of AMI as assessed by the LVEF and the rise of CK-MB.

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Section: Introductionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

The role of cytokines and cortisol in the non-thyroidal illness syndrome following acute myocardial infarction

Karga

Papaioannou

Venetsanou

et al. 2000

European Journal of Endocrinology

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“…This is consistent with the previous results showing depletion of circulating leukocytes and loss of IL-8 immunoreactivity in postischemic myocardial tissue. 54 It is well known that IL-8 is a potent chemoattractant and activator of neutrophils. 55,56 Therefore, IL-8 produced by neutrophils infiltrating the infarcted myocardium might be responsible for subsequent accumulation and activation of neutrophils, leading to an increase in myocardial cell damage due to the neutrophil-mediated microvascular obstruction.…”

Section: Discussionmentioning

confidence: 99%

Myocardial apoptosis associated with the expression of proinflammatory cytokines during the course of myocardial infarction

et al. 2006

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To clarify the role of myocardial apoptosis associated with the expression of proinflammatory cytokines in human myocardial infarction (MI), we have analyzed the expression of apoptosis positive for single-stranded DNA (ss-DNA) antibody, tumor necrosis factor (TNF)-a, and interleukin (IL)-8 in 147 samples of infarcted myocardial tissue from 65 patients. ss-DNA-positive apoptotic nuclei were found mainly in cardiomyocytes in the border zones and granulation tissue cells in the infarct foci. The ss-DNA index (SI) of cardiomyocytes (average 0.13%) peaked at stage II (established myocardial necrosis), the value being significantly higher than at stages III (macrophage infiltration), IV (granulation formation), and V (scar formation) (Po0.05), whereas the SI of granulation tissue (average 0.08%) at stages III, IV, and V showed no significant differences between the three stages. These results suggest that cardiomyocyte apoptosis in the border zone is responsible for cellular loss in the acute stage of MI, whereas granulation tissue apoptosis may not be involved in the process of ventricular remodeling. TNF-a was expressed in cardiomyocytes in the border zones of infarct foci, but no significant positive correlation was found between SI and TNF-a index in cardiomyocytes (r ¼ 0.08, P ¼ 0.37), suggesting that TNF-a does not serve as a direct trigger of cardiomyocyte apoptosis in vivo. The number of IL-8-positive cells peaked at stage II, and IL-8-myeloperoxidase-double-positive neutrophils were frequently detected, indicating that infiltrating neutrophils are the predominant source of IL-8 in the infarcted myocardium. These results suggest that, in human MI, TNF-a produced by cardiomyocytes does not play a critical role in their apoptosis, and that IL-8 produced by neutrophils is responsible for the subsequent accumulation and activation of neutrophils, thus increasing the degree of myocardial damage.

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“…Total RNA of 10 7 ECV-304 cells or 2.5ϫ10 7 mononuclear cells was isolated with the RNeasy Mini Kit (Qiagen GmbH) and analyzed by Northern blotting as described previously. 25 Briefly, 5 g of total RNA of each sample was subjected to electrophoresis on a 1.2% agarose gel containing 100 mmol/L MOPS (Boehringer), 40 mmol/L sodium acetate (Boehringer), 5 mmol/L EDTA, and 6% formaldehyde (Boehringer). The RNA was transferred to nylon membrane (Hybond-N, Amersham) in 20ϫ SSC (Merck) by capillary blotting overnight.…”

Section: Rna Preparation Northern Blot Analysis and Electrophoreticmentioning

confidence: 99%

Adhesion of Monocyte Very Late Antigen-4 to Endothelial Vascular Cell Adhesion Molecule-1 Induces Interleukin-1β–Dependent Expression of Interleukin-6 in Endothelial Cells

Zohlnhöfer

Brand

Schipek

et al. 2000

ATVB

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Abstract-In atheroma, T cell-derived interferon-␥ (INF-␥) stimulates endothelial cells and facilitates recruitment of monocytes. We investigated potential mechanisms by which these interactions could contribute to local and systemic inflammatory responses. Specifically, we analyzed the expression of interleukin (IL)-1␤ and IL-6 in both cell types after coculture, the relevant adhesion molecules in this interaction, and transcriptional control by NF-B. We studied coculture of purified peripheral blood monocytes with human umbilical vein endothelial cells (

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Induction of Cytokine Expression in Leukocytes in Acute Myocardial Infarction

Abstract: Plasma from the ischemic and reperfused heart stimulates the expression of IL-1 beta and IL-8 in leukocytes. Therefore, leukocyte-derived cytokines may contribute to the regulation of cardiac inflammatory responses in patients with an acute MI.

Cited by 124 publications

References 31 publications

The role of cytokines and cortisol in the non-thyroidal illness syndrome following acute myocardial infarction

The role of cytokines and cortisol in the non-thyroidal illness syndrome following acute myocardial infarction

Myocardial apoptosis associated with the expression of proinflammatory cytokines during the course of myocardial infarction

Adhesion of Monocyte Very Late Antigen-4 to Endothelial Vascular Cell Adhesion Molecule-1 Induces Interleukin-1β–Dependent Expression of Interleukin-6 in Endothelial Cells

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