Characterization of Cytokine and iNOS mRNA Expression in situ During the Course of Experimental Autoimmune Myocarditis in Rats

Okura, Yuji; Yamamoto, Tadashi; Goto, Shin; Inomata, Takayuki; Hirono, Shuichi; Hanawa, Haruo; Li, Feng; Wilson, Curtis B.; Kihara, Itaru; Izumi, Tohru; Shibata, Akira; Aizawa, Yoshifusa; Seki, Shu; Abo, Toru

doi:10.1006/jmcc.1996.0293

Cited by 109 publications

(100 citation statements)

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“…Histolog- KOHNO, ET AL ical examination showed inflammatory cells around the cardiac muscle cells undergoing necrosis ( Figure 5). This inflammation was essentially the same as in previous reports 6,10,11) except for enhanced severity. On the other hand, the SmaI excised PstI fragment or the control (PBS+CFA) was totally devoid of any inflammatory changes ( Figure 5).…”

Section: Resultssupporting

confidence: 86%

Advantage of Recombinant Technology for the Identification of Cardiac Myosin Epitope of Severe Autoimmune Myocarditis in Lewis Rats.

et al. 2000

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SUMMARYWhole cardiac myosin induced experimental autoimmune myocarditis (EAM) in animals. The identification of the epitope causing EAM is expected to elucidate the mechanism leading to the onset of this autoimmune disease. Until now such studies have been done mostly with synthetic oligo-peptides. We employed recombinant technology to produce the immunogenic fragment of the self-cardiac myosin heavy chain (CMHC) for EAM in Lewis rats, and successfully induced severe myocarditis with short recombinant peptide fragment CMHC residues 1107 to 1186. The immunogenicity was completely abolished from the fragment with futher excision of 12 amino acids from residues 1131 to 1143. This recombinant technology clearly has advantages in the ease of manipulation and the purity for the creation of immunogenic epitopes. (Jpn Heart J 2000; 41: 67-77)

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Section: Resultssupporting

confidence: 86%

Advantage of Recombinant Technology for the Identification of Cardiac Myosin Epitope of Severe Autoimmune Myocarditis in Lewis Rats.

et al. 2000

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“…98 TNF-␣ is believed to be produced by heartinfiltrating macrophages in the rat model of myocarditis and to be important in cardiovascular diseases. 99 It has been reported that the lack of TNF-␣ receptor (TNF-R) p55 gene expression could interfere with either lymphocyte activation or target organ susceptibility. 100 In fact, A/J mice lacking TNF-R p55 are susceptible to Listeria infections, 101 but were protected from cardiac myosininduced myocarditis.…”

Section: Influence Of Cytokines On Myocarditis and Th1/ Th2 Immune Rementioning

confidence: 99%

Cardiac Myosin and the TH1/TH2 Paradigm in Autoimmune Myocarditis

Cunningham

2001

The American Journal of Pathology

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“…Interleukin (IL)-10 is an anti-inflammatory cytokine that binds to specific IL-10 receptors located on mast cells and prevents the release of inflammatory mediators [24]. This immunomodulatory cytokine plays an important role in the recovery from EAM by inhibiting pro-inflammatory T helper type 1 cells, macrophages and cytokines [25][26][27].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of mast cells by interleukin‐10 gene transfer contributes to protection against acute myocarditis in rats

Palaniyandi

Watanabe

et al. 2004

Eur J Immunol

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Progression of acute myocarditis involves a variety of inflammatory events. Mast cells have been implicated as the source of various cytokines, chemokines and histamine in acute inflammation and fibrosis. Interleukin (IL)-10 has well-known immunomodulatory actions that are exerted during the recovery phase of myocarditis. In this study, 9-week-old male Lewis rats were immunized with cardiac myosin. A plasmid vector expressing mouse IL-10 cDNA (800 lg per rat) was then transferred three times (7, 12 and 17 days after immunization) into the tibialis anterior muscles of the rats by electroporation. Microscopic examination of mast cells was carried out on toluidine blue-stained transverse sections of the mid ventricles. Mouse IL-10 gene transfer significantly reduced mast cell density, cardiac histamine concentration and mast cell growth, and prevented mast cell degranulation. Furthermore, improvement in both myocardial function and the overall condition of the rats was evident from the reduction in the heart weight-to-body weight ratio and inflammatory infiltration as well as improvement in hemodynamic and echocardiographic parameters. These findings suggest that IL-10 gene transfer by electroporation protected against myocarditis via mast cell inhibition.

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Characterization of Cytokine and iNOS mRNA Expression in situ During the Course of Experimental Autoimmune Myocarditis in Rats

Cited by 109 publications

References 0 publications

Advantage of Recombinant Technology for the Identification of Cardiac Myosin Epitope of Severe Autoimmune Myocarditis in Lewis Rats.

Advantage of Recombinant Technology for the Identification of Cardiac Myosin Epitope of Severe Autoimmune Myocarditis in Lewis Rats.

Cardiac Myosin and the TH1/TH2 Paradigm in Autoimmune Myocarditis

Inhibition of mast cells by interleukin‐10 gene transfer contributes to protection against acute myocarditis in rats

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