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  1. Article ; Online: Heart disease in a mutant mouse model of spontaneous eosinophilic myocarditis maps to three loci.

    Zimmermann, Nives / Gibbons, William J / Homan, Shelli M / Prows, Daniel R

    BMC genomics

    2019  Volume 20, Issue 1, Page(s) 727

    Abstract: Background: Heart disease (HD) is the major cause of morbidity and mortality in patients with hypereosinophilic diseases. Due to a lack of adequate animal models, our understanding of the pathophysiology of eosinophil-mediated diseases with heart ... ...

    Abstract Background: Heart disease (HD) is the major cause of morbidity and mortality in patients with hypereosinophilic diseases. Due to a lack of adequate animal models, our understanding of the pathophysiology of eosinophil-mediated diseases with heart complications is limited. We have discovered a mouse mutant, now maintained on an A/J inbred background, that spontaneously develops hypereosinophilia in multiple organs. Cellular infiltration into the heart causes an eosinophilic myocarditis, with affected mice of the mutant line (i.e., A/J
    Results: Maintaining the A/J
    Conclusions: These results indicate the HD trait in this mutant mouse model of eosinophilic myocarditis is oligogenic with variable penetrance, due to multiple segregating variants and possibly additional genetic or nongenetic factors. The A/J
    MeSH term(s) Animals ; Chromosome Mapping/methods ; Chromosomes, Mammalian/genetics ; Disease Models, Animal ; Eosinophilia/genetics ; Eosinophilia/mortality ; Female ; Genetic Linkage ; Genetic Loci ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mutation ; Myocarditis/genetics ; Myocarditis/mortality ; Penetrance
    Language English
    Publishing date 2019-10-11
    Publishing country England
    Document type Journal Article
    ISSN 1471-2164
    ISSN (online) 1471-2164
    DOI 10.1186/s12864-019-6108-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Characterization of a mouse model of hypereosinophilia-associated heart disease.

    Prows, Daniel R / Klingler, Andrea / Gibbons, William J / Homan, Shelli M / Zimmermann, Nives

    American journal of physiology. Heart and circulatory physiology

    2019  Volume 317, Issue 2, Page(s) H405–H414

    Abstract: Hypereosinophilic syndrome is characterized by sustained and marked eosinophilia leading to tissue damage and organ dysfunction. Morbidity and mortality occur primarily due to cardiac and thromboembolic complications. Understanding the cause and ... ...

    Abstract Hypereosinophilic syndrome is characterized by sustained and marked eosinophilia leading to tissue damage and organ dysfunction. Morbidity and mortality occur primarily due to cardiac and thromboembolic complications. Understanding the cause and mechanism of disease would aid in the development of targeted therapies with greater efficacy and fewer side effects. We discovered a spontaneous mouse mutant in our colony with a hypereosinophilic phenotype. Mice develop peripheral blood eosinophilia; infiltration of lungs, spleen, and heart by eosinophils; and extensive myocardial damage and remodeling. This ultimately leads to heart failure and premature death. Histopathological assessment of the hearts revealed a robust inflammatory infiltrate composed primarily of eosinophils and B-lymphocytes, associated with myocardial damage and replacement fibrosis, consistent with eosinophilic myocarditis. In many cases, hearts showed dilatation and thinning of the right ventricular wall, suggestive of an inflammatory dilated cardiomyopathy. Most mice showed atrial thrombi, which often filled the chamber. Protein expression analysis revealed overexpression of chemokines and cytokines involved in innate and adaptive immunity including IL-4, eotaxin, and RANTES. Disease could be transferred to wild-type mice by adoptive transfer of splenocytes from affected mice, suggesting a role for the immune system. In summary, the pathologies observed in the mutant lines are reminiscent of those seen in patients with hypereosinophilia, where cardiac-related morbidities, like congestive heart failure and thrombi, are the most common causes of death. As such, our model provides an opportunity to test mechanistic hypotheses and develop targeted therapies.
    MeSH term(s) Adaptive Immunity ; Animals ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Cardiomyopathy, Dilated/etiology ; Cardiomyopathy, Dilated/immunology ; Cardiomyopathy, Dilated/metabolism ; Cardiomyopathy, Dilated/pathology ; Cytokines/immunology ; Cytokines/metabolism ; Disease Models, Animal ; Disease Progression ; Eosinophils/immunology ; Eosinophils/metabolism ; Fibrosis ; Genetic Predisposition to Disease ; Heart Failure/etiology ; Heart Failure/immunology ; Heart Failure/metabolism ; Heart Failure/pathology ; Hypereosinophilic Syndrome/complications ; Hypereosinophilic Syndrome/immunology ; Hypereosinophilic Syndrome/metabolism ; Hypereosinophilic Syndrome/pathology ; Immunity, Innate ; Mice, Mutant Strains ; Myocarditis/etiology ; Myocarditis/immunology ; Myocarditis/metabolism ; Myocarditis/pathology ; Myocardium/immunology ; Myocardium/metabolism ; Myocardium/pathology ; Phenotype ; Signal Transduction ; Time Factors ; Ventricular Remodeling
    Chemical Substances Cytokines
    Language English
    Publishing date 2019-06-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00133.2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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