Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis

Nishii, Mototsugu; Inomata, Takayuki; Takehana, Hitoshi; Takeuchi, Ichiro; Nakano, Hironari; Koitabashi, Toshimi; Nakahata, Junichi; Aoyama, Naoyoshi; Izumi, Tohru

doi:10.1016/j.jacc.2004.01.055

Cited by 70 publications

(44 citation statements)

References 23 publications

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“…37 In patients with fulminant myocarditis, elevated IL-10 serum levels were observed, 38 which is in agreement with our observation in mice during the acute phase of CVB3 myocarditis. In these patients, IFN-␥ levels were not increased, 38 so the fatal outcome in one third of the patients, who had the highest IL-10 levels, is plausible. In addition, iNOS activity was found to be present in patients with myocarditis and dilated cardiomyopathy.…”

Section: Discussionsupporting

confidence: 87%

Sustained Nitric Oxide Synthesis Contributes to Immunopathology in Ongoing Myocarditis Attributable to Interleukin-10 Disorders

Szalay

Sauter

Hald

et al. 2006

The American Journal of Pathology

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Ongoing coxsackievirus B3 (CVB3) myocarditis is characterized by persistence of viral RNA and chronic inflammation primarily mediated by macrophages and T cells. Activated macrophages produce anti-viral effector molecules comprising reactive nitrogen intermediates; however, reactive nitrogen intermediates also contribute to host tissue damage. Controlled activation of macrophages depends on interferon (IFN)-␥ and interleukin (IL)-10. To evaluate mechanisms involved in CVB3-induced pathogenesis of myocarditis, we determined the relationship of inducible nitric-oxide synthase (iNOS) mRNA expression with IFN-␥ and IL-10 secretion during CVB3 infection in different mouse strains. We found in susceptible A.BY/SnJ mice that develop ongoing myocarditis, a low and delayed IFN-␥ secretion and highly diminished IL-10 production compared with resistant C57BL/6 mice. Consequently, iNOS mRNA synthesis was delayed but clearly prolonged in susceptible mice. IL-10 gene-deficient mice confirmed the regulatory role of IL-10 in the outcome of CVB3 myocarditis. These mice did not establish a persistent cardiac infection and revealed IFN-␥ secretion kinetics similar to resistant mice but showed a slightly elongated cardiac iNOS mRNA expression resulting in extended myocarditis. We conclude that coordinated secretion of IFN-␥ and IL-10 is crucial for the effective resolution of CVB3 myocarditis. Moreover, lack of regulatory IL-10 leads to uncontrolled iNOS mRNA production, thus contributing to ongoing myocardial injury. The natural course of human enterovirus myocarditis varies from a subclinical infection to fulminant acute myocarditis with congestive heart failure. Susceptible patients may develop a chronic inflammatory heart disease leading to dilated cardiomyopathy, which in its end stage can be treated effectively only by heart transplantation.

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Section: Discussionsupporting

confidence: 87%

Sustained Nitric Oxide Synthesis Contributes to Immunopathology in Ongoing Myocarditis Attributable to Interleukin-10 Disorders

Szalay

Sauter

Hald

et al. 2006

The American Journal of Pathology

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“…1 Some patients, however, progress to persistent myocardial inflammation and subsequent dilated cardiomyopathy. 2,3 Although chronic viral infection has long been recognized as a candidate causative factor for these pathophysiological mechanisms, 3 a number of experimental models have demonstrated the crucial role 4,5 of myocardial structure-mediated autoimmune processes, which follow the myocardial damage provoked by the initial viral infection.…”

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confidence: 99%

β2-Adrenergic Agonists Suppress Rat Autoimmune Myocarditis

et al. 2006

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Background-The therapeutic potential of ␤2-adrenergic receptor (AR) agonists in the treatment of autoimmune diseases has been reported. However, the role of these drugs in the myocardial structure-induced autoimmune process, which is thought to play a crucial role in the progression of myocarditis to subsequent complications, has not been elucidated. Methods and Results-Experimental autoimmune myocarditis (EAM) was induced in rats by immunization with cardiac myosin. On daily administration from day 0 after immunization, the ␤2-selective AR agonists formoterol or salbutamol ameliorated EAM on day 21 and increased myocardial interleukin-10/interferon-␥ mRNA levels. Propranolol, a nonselective ␤-AR antagonist, aggravated EAM on day 21 and decreased mRNA levels, whereas metoprolol, a ␤1-selective AR antagonist, showed no effect. These results were reflected in vivo by the proliferation of cardiac myosin-primed lymph node cells from drug-treated rats. In vitro addition of ␤2-selective AR agonists inhibited the activation of cardiac myosin fragment-specific myocarditogenic T lymphocytes, and this effect was reversed by ICI118,551, a ␤2-selective AR antagonist. Furthermore, treatment with 2 different ␤2-selective AR agonists starting on day 14 also ameliorated EAM on day 21. Conclusions-␤2-AR

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“…The sensitivity of the electrocardiogram for myocarditis is low (47%). 20 The presence of Q waves or left bundle-branch block is associated with higher rates of death or cardiac transplantation. 21 Echocardiography is useful primarily to rule out other causes of heart failure, since there are no specific features of acute myocarditis.…”

Section: Diagnosismentioning

confidence: 99%

Myocarditis-A Quick Review

Prasad¹,

Kumar²

2017

IOSR JDMS

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Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis

Abstract: Serum IL-10 levels on admission enabled one to predict subsequent CS requiring MCSS and mortality of fulminant myocarditis patients.

Cited by 70 publications

References 23 publications

Sustained Nitric Oxide Synthesis Contributes to Immunopathology in Ongoing Myocarditis Attributable to Interleukin-10 Disorders

Sustained Nitric Oxide Synthesis Contributes to Immunopathology in Ongoing Myocarditis Attributable to Interleukin-10 Disorders

β2-Adrenergic Agonists Suppress Rat Autoimmune Myocarditis

Myocarditis-A Quick Review

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