Role of oxygen derived free radicals in the pathogenesis of coxsackievirus B3 myocarditis in mice

Hiraoka, Yuji; Kishimoto, Chiharu; Takada, Hitoshi; Kurokawa, Mineo; Ochiai, Hiroshi; Shiraki, Kimíyasu; Sasayama, Shígetake

doi:10.1093/cvr/27.6.957

Cited by 42 publications

(16 citation statements)

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“…Portions of the heart were homogenized aseptically, and plaque assay was performed, as previously described. 5,6 Histopathology…”

Section: Experimental Infectionmentioning

confidence: 99%

“…The myocardial lesions were graded semiquantitatively on a scale of +1 to +4. 5,6 The histopathological criteria for grading the severity of infiltration and necrosis were grade 1 (mild), 1 or 2 small foci; grade 2 (slight), several small foci; grade 3 (moderate), multiple small foci or several large foci; and grade 4 (severe), multiple large foci, diffuse infiltration, or necrosis.…”

Section: Experimental Infectionmentioning

confidence: 99%

“…8 Oxygen free radicals may be involved in the pathogenesis and development of coxsackievirus B3 myocarditis and so appropriate dosages of superoxide dismutase have therapeutic potential for myocarditis. 6,7 However, it has not been reported whether viral myocarditis is controlled by the redox regulatory protein, TRX and so the present study investigated whether the cellular redox regulation in immune-mediated myocarditis, coxsackievirus B3 myocarditis, was induced in various strains of mice, and what is the role of cellular redox state in the development of viral myocarditis.…”

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confidence: 97%

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Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice

Miyamoto¹,

Kishimoto²,

Shioji³

et al. 2001

Jpn Circ J

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“…Portions of the heart were homogenized aseptically, and plaque assay was performed, as previously described. 5,6 Histopathology…”

Section: Experimental Infectionmentioning

confidence: 99%

Section: Experimental Infectionmentioning

confidence: 99%

mentioning

confidence: 97%

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Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice

Miyamoto¹,

Kishimoto²,

Shioji³

et al. 2001

Jpn Circ J

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“…Increasing evidence suggests that cytotoxic T cells (8,9), neurohumoral factors (17), and free radicals (4,5), possibly generated by infiltrating cells in the myocardium, play a significant role, separately or together, in the development of myocardial damage and dysfunction, in addition to the primary damage caused by viral infection. Inflammatory cytokines are also involved in the pathogenesis of myocardial injury in viral myocarditis (6,11).…”

mentioning

confidence: 99%

Enhanced Production of Macrophage Inflammatory Protein 2 (MIP-2) by In Vitro and In Vivo Infections with Encephalomyocarditis Virus and Modulation of Myocarditis with an Antibody against MIP-2

Kishimoto

Kawamata²,

Sakai³

et al. 2001

J Virol

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Interleukin-8 (IL-8) is a chemotactic cytokine for neutrophils and lymphocytes. Macrophage inflammatory protein 2 (MIP-2) is a murine counterpart of IL-8. The present study was performed to determine whether MIP-2 aggravates murine myocarditis. We examined (i) the MIP-2-producing activity of encephalomyocarditis (EMC) virus-infected cultured macrophages, (ii) serial plasma MIP-2 levels in EMC virus-induced mice by enzyme-linked immunosorbent assay, and (iii) the effects of antimouse MIP-2 monoclonal antibody (MAb) in vivo upon myocarditis. The production of MIP-2 increased in an infection dose-and time-dependent manner in virus-infected RAW 264.7 macrophages. Five-week-old C 3 H/He mice were inoculated with EMC virus. Plasma MIP-2 levels were significantly elevated in mice on days 7 and 14 postinfection. Mice were injected subcutaneously with anti-MIP-2 MAb at 10 g/day (group 2) or 100 g/day (group 3) on days 0 to 5 and were observed until day 21. Uninfected control mice (group 1) were prepared. The survival rate was higher in the anti-MIP-2-treated group (group 3), but not in group 2, than in the control group. Histopathological analysis revealed that cellular infiltration and myocardial necrosis with macrophage and T-cell accumulation were less prominent in the anti-MIP-2 MAb-treated group, but not in group 2, compared to the level in the controls. MIP-2 is an important naturally occurring inflammatory cytokine in myocarditis, and anti-MIP-2 MAb treatment may prevent the inflammatory response.

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“…As shown in animal models, oxygen free radicals may also contribute to the pathogenesis of infectious myocarditis. 26,27 In homozygous β-thalassemia, organ damage is mainly attributed to excessive iron deposition through the formation of free radicals. Beta-thalassemia major patients without left-sided heart failure have an apolipoprotein Eε4 allele frequency similar to that of healthy controls, while patients with left-sided heart failure have a high frequency of this allele relative to controls.…”

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confidence: 99%

Heart Failure in β‐Thalassemia

Kremastinos

2001

Congestive Heart Failure

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Heart failure remains the main cause of death in ß-thalassemia despite the progress that has been made. Myocardial Heart failure remains the main cause of death in β-thalassemia, despite the progress that has been made by intensification of iron chelation therapy. 1 It has been traditionally considered the result of iron overload due to regular blood transfusions, intestinal iron hyperabsorption, and ineffective erythropoiesis during a patient's lifespan. 2,3 Regular, intense chelation therapy has improved quality of life and the survival rate by decreasing the secondary hemochromatosis. However, heart failure is not prevented by intensification of iron chelation therapy. 4,5 It can thus be hypothesized that either deferoxamine is less effective than is believed or other factors might be involved in the pathogenesis of the heart failure.Beta-thalassemia is not a pure iron storage disease and the pathophysiology of cardiac dysfunction is poorly understood and multifactorial in etiology. 6,7 Left-sided and subsequently biventricular heart failure appear early in the patients' life. This is the most common mode of heart failure in this disease, which is characterized at diagnosis by left ventricular systolic dysfunction, dilatation, and failure. 2,[8][9][10] Chronic myocardial iron deposition does not affect left ventricular relaxation but causes left ventricular myocardial restriction, with highly elevated pulmonary arteriolar resistance and pressure. It appears in the elderly β-thalassemia major population, who have the highest serum ferritin levels. These patients eventually develop right ventricular dilatation, while left ventricular dimensions and systolic function remain within the normal range. This is the pre-heart failure stage, with predominant symptoms and signs of right-sided heart failure. 11 In 1964, Engle et al. 8 first reported the coexistence of pericarditis and fatal arrhythmias with heart failure in β-thalassemia major. Of note, pericarditis usually coincides to some degree with myocarditis, an inflammatory heart disease that usually has an immunologic background. 2,12,13 Years later, our group 14 showed that acute infectious myocarditis in β-thalassemia major, in addition to causing acute failure, also caused chronic leftsided heart failure in 27.6% of myocarditis patients within approximately 3.5 years, compared to an ageand sex-matched β-thalassemic population with no difference in iron loading. The estimated prevalence of overt myocarditis in β-thalassemia was 4.5% in a population with clinical evidence of myopericarditis documented mainly by myocardial biopsy.

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Role of oxygen derived free radicals in the pathogenesis of coxsackievirus B3 myocarditis in mice

Cited by 42 publications

References 0 publications

Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice

Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice

Enhanced Production of Macrophage Inflammatory Protein 2 (MIP-2) by In Vitro and In Vivo Infections with Encephalomyocarditis Virus and Modulation of Myocarditis with an Antibody against MIP-2

Heart Failure in β‐Thalassemia

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