Models of coxsackievirus-B3-induced myocarditis: recent advances

Fairweather, De Lisa; Rose, Noel R.

doi:10.1016/j.ddmod.2004.11.003

Cited by 9 publications

(12 citation statements)

References 31 publications

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“…Fibroblasts are a major component of cardiac tissue and so it is not surprising that fibrosis is an important contributor to the development of DCM and congestive heart failure (38,39). In our model of CVB3-induced myocarditis, fibrosis is not observed during acute myocarditis but develops with the progression to chronic disease (14,28,40). In this study, we observed increased fibrotic pericarditis during acute CVB3 myocarditis (day 10 or 12 p.i.)…”

Section: Cr1/2 Deficiency Increases Pericardial Fibrosissupporting

confidence: 52%

“…and progress to develop chronic autoimmune myocarditis and DCM (days 35 to 56 p.i.) (13,14). In this study, we found survival was reduced by ϳ50% on days 7-8 p.i.…”

Section: Cr1/2 Deficiency Reduces Survival Following Cvb3 Infectionmentioning

confidence: 59%

“…), but develops in susceptible strains of mice (i.e., BALB/c and A/J) by day 35 p.i. during chronic myocarditis (14,28). We previously reported that DCM is more severe in mice deficient in IFN-␥ during chronic CVB3-induced myocarditis or EAM, and is associated with increased heart failure and death (28,32,33).…”

Section: Cr1/2 Deficiency Increases Dcmmentioning

confidence: 99%

“…Myocarditis is a principal cause of heart disease in young adults and is often a precursor of heart failure due to the progression to dilated cardiomyopathy (DCM) (11,12). Coxsackievirus B3 (CVB3) infection of susceptible A/J or BALB/c mice results in a disease similar to that observed in humans, with the development of acute myocarditis from days 7 to 14 after infection that progresses to chronic myocarditis and DCM from day 28 to at least day 58 after infection (13,14). The pathogenesis of myocarditis involves both T cell-mediated and Ab-mediated mechanisms (15)(16)(17), with IgG Ab and C deposition in the hearts of patients with DCM or A/J mice inoculated with cardiac myosin and adjuvant to induce experimental autoimmune myocarditis (EAM) (18 -21).…”

mentioning

confidence: 99%

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Complement Receptor 1 and 2 Deficiency Increases Coxsackievirus B3-Induced Myocarditis, Dilated Cardiomyopathy, and Heart Failure by Increasing Macrophages, IL-1β, and Immune Complex Deposition in the Heart

Fairweather

Frisancho-Kiss

Njoku

et al. 2006

The Journal of Immunology

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Complement and complement receptors (CR) play a central role in immune defense by initiating the rapid destruction of invading microorganisms, amplifying the innate and adaptive immune responses, and mediating solubilization and clearance of immune complexes. Defects in the expression of C or CR have been associated with loss of tolerance to self proteins and the development of immune complex-mediated autoimmune diseases such as systemic lupus erythematosus. In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice deficient in CR1/2. We found that CR1/2 deficiency significantly increased acute CVB3 myocarditis and pericardial fibrosis resulting in early progression to dilated cardiomyopathy and heart failure. The increase in inflammation was not due to increased viral replication, which was not significantly altered in the hearts of CR1/2-deficient mice, but was associated with increased numbers of macrophages, IL-1β levels, and immune complex deposition in the heart. The complement regulatory protein, CR1-related gene/protein Y (Crry), was increased on cardiac macrophage populations, while immature B220low B cells were increased in the spleen of CR1/2-deficient mice during acute CVB3-induced myocarditis. These results show that expression of CR1/2 is not necessary for effective clearance of CVB3 infection, but prevents immune-mediated damage to the heart.

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Section: Cr1/2 Deficiency Increases Pericardial Fibrosissupporting

confidence: 52%

“…and progress to develop chronic autoimmune myocarditis and DCM (days 35 to 56 p.i.) (13,14). In this study, we found survival was reduced by ϳ50% on days 7-8 p.i.…”

Section: Cr1/2 Deficiency Reduces Survival Following Cvb3 Infectionmentioning

confidence: 59%

Section: Cr1/2 Deficiency Increases Dcmmentioning

confidence: 99%

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confidence: 99%

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Complement Receptor 1 and 2 Deficiency Increases Coxsackievirus B3-Induced Myocarditis, Dilated Cardiomyopathy, and Heart Failure by Increasing Macrophages, IL-1β, and Immune Complex Deposition in the Heart

Fairweather

Frisancho-Kiss

Njoku

et al. 2006

The Journal of Immunology

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“…Currently, several animal models are available that closely resemble human myocarditis [7]. Murine models fall into two basic categories: acute cardiac inflammation and sudden death induced by direct viral damage (where nearly 70% of animals die at day 4 to 7 after infection) [8][9][10][11], or inflammation triggered by adjuvant and cardiac myosin or virus and cardiac myosin (heart-passaged virus) resulting in acute myocarditis with no deaths that progresses to chronic heart disease and DCM [5,6,[12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Coxsackievirus-induced myocarditis in mice: A model of autoimmune disease for studying immunotoxicity

Fairweather¹,

Rose²

2007

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Excellent animal models are available of virus-induced and autoimmune heart disease that are remarkably similar to human disease. Developing good animal models for heart disease is crucial because cardiovascular disease is now the leading cause of death in the United States and is estimated to be the leading cause of death in the world by the year 2020. A significant proportion of heart disease in Western populations is associated with inflammation. Myocarditis, or inflammation of the heart muscle, is the major cause of sudden death in young adults. Although most individuals recover from acute myocarditis, genetically susceptible individuals may go on to develop chronic myocarditis and dilated cardiomyopathy (DCM) resulting in congestive heart failure. In this article, we describe a model of autoimmune myocarditis and DCM induced by inoculation with heart-passaged coxsackievirus B3 (CVB3). Intraperitoneal inoculation of susceptible mice with CVB3 induces acute cardiac inflammation from days 7 to 14 post infection (pi) that progresses to chronic myocarditis and DCM from day 28 to at least 56 pi. The model of CVB3-induced myocarditis presented here allows dissection of the contribution of viral infection and xenobiotics on immune dysregulation and inflammation in the heart. An improved understanding of the interaction between environmental exposures and the development of heart disease represents a clear challenge for immunotoxicologists.

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Autoimmune Myocarditis, Valvulitis, and Cardiomyopathy

et al. 2013

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Cardiac myosin-induced autoimmune myocarditis (EAM) is a model of inflammatory heart disease initiated by CD4+ T cells (Smith and Allen 1991; Li, Heuser et al. 2004). It is a paradigm of the immune-mediated cardiac damage believed to play a role in the pathogenesis of a subset of postinfectious human cardiomyopathies (Rose, Herskowitz et al. 1993). Myocarditis is induced in susceptible mice by immunization with purified cardiac myosin (Neu, Rose et al. 1987) or specific peptides derived from cardiac myosin (Donermeyer, Beisel et al. 1995; Pummerer, Luze et al. 1996) (see Basic Protocol 1), or by adoptive transfer of myosin-reactive T cells (Smith and Allen 1991) (see Alternate Protocol). Myocarditis has been induced in Lewis rats by immunization with purified rat or porcine cardiac myosin (Kodama, Matsumoto et al. 1990; Li, Heuser et al. 2004) (see Basic Protocol 2) or S2-16 peptide (Li, Heuser et al. 2004), or by adoptive transfer of T cells stimulated by specific peptides derived from cardiac myosin (Wegmann, Zhao et al. 1994). Myocarditis begins 12 to 14 days after the first immunization, and is maximal after 21 days. Other animal models commonly used to study myocarditis development include the pathogen-induced models in which disease is initiated by viral infection. The first murine model of acute viral myocarditis causes sudden death via viral damage to cardiomyocytes (Huber, Gauntt et al. 1998; Horwitz, La Cava et al. 2000; Fong 2003; Fuse, Chan et al. 2005; Fairweather and Rose 2007; Cihakova and Rose 2008) whereas the second model is based on inoculation with heart-passaged coxsackievirus B3 (CVB3) that includes damaged heart proteins (Fairweather, Frisancho-Kiss et al. 2004; Fairweather D 2004; Fairweather and Rose 2007; Cihakova and Rose 2008) In addition to the protocols used to induce EAM in mice and rats, support protocols are included for preparing purified cardiac myosin using mouse or rat heart tissue (see Support Protocol 1), preparing purified cardiac myosin for injection (see Support Protocol 2), and collecting and assessing hearts by histopathological means (see Support Protocol 3).

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Models of coxsackievirus-B3-induced myocarditis: recent advances

Cited by 9 publications

References 31 publications

Complement Receptor 1 and 2 Deficiency Increases Coxsackievirus B3-Induced Myocarditis, Dilated Cardiomyopathy, and Heart Failure by Increasing Macrophages, IL-1β, and Immune Complex Deposition in the Heart

Complement Receptor 1 and 2 Deficiency Increases Coxsackievirus B3-Induced Myocarditis, Dilated Cardiomyopathy, and Heart Failure by Increasing Macrophages, IL-1β, and Immune Complex Deposition in the Heart

Coxsackievirus-induced myocarditis in mice: A model of autoimmune disease for studying immunotoxicity

Autoimmune Myocarditis, Valvulitis, and Cardiomyopathy

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