Literature DB >> 8575737

Rheumatic Aschoff nodules revisited: an immunohistological reappraisal of the cellular component.

W J Fraser1, Z Haffejee, K Cooper.   

Abstract

Rheumatic fever is still the leading cause of acquired heart disease in children and young adults in developing countries. Recent reports have documented a rising incidence of rheumatic fever in both the USA and Europe. The disease is characterized by specific lesions in the heart muscle and valves called Aschoff nodules. The Aschoff nodule has been neglected in the last few decades as most of the studies were conducted in the 1960s on autopsy tissues. This study examines Aschoff nodules using heart valve material obtained at valve surgery with updated commercially available immunohistochemical antibodies to determine the phenotypic characteristics of the cells involved in the formation of these lesions. Fifteen cases of rheumatic valvulitis, as indicated by the presence of Aschoff nodules, were examined. The Anitschkow and Aschoff cells stained prominently with macrophage markers. Three stages of nodules with Aschoff and Anitschkow cells were identified: stage 1, central fibrinoid necrosis without lymphocytes, stage 2 with occasional T lymphocytes (< 10) and stage 3 with lymphoid aggregates containing both T- and B-lymphocytes (with occasional admixed macrophages). We propose that the stage 1 lesion is the earliest granulomatous stage with the lymphoid aggregates being a later stage in the development of Aschoff nodules. The Aschoff and Anitschkow cells demonstrated mitotic activity and stained with antibodies to the proliferation cell nuclear antigen (PCNA) suggesting that the multinucleated giant cells may be formed, at least partially, by nuclear division rather than fusion.

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Year:  1995        PMID: 8575737     DOI: 10.1111/j.1365-2559.1995.tb00310.x

Source DB:  PubMed          Journal:  Histopathology        ISSN: 0309-0167            Impact factor:   5.087


  6 in total

Review 1.  Role of NADPH oxidase in formation and function of multinucleated giant cells.

Authors:  Mark T Quinn; Igor A Schepetkin
Journal:  J Innate Immun       Date:  2009-07-07       Impact factor: 7.349

2.  B- and T-cell responses in group a streptococcus M-protein- or Peptide-induced experimental carditis.

Authors:  Davina Gorton; Brenda Govan; Colleen Olive; Natkunam Ketheesan
Journal:  Infect Immun       Date:  2009-03-09       Impact factor: 3.441

3.  Transgenic overexpression of platelet-derived growth factor-C in the mouse heart induces cardiac fibrosis, hypertrophy, and dilated cardiomyopathy.

Authors:  Annica Pontén; Xuri Li; Peter Thorén; Karin Aase; Tobias Sjöblom; Arne Ostman; Ulf Eriksson
Journal:  Am J Pathol       Date:  2003-08       Impact factor: 4.307

4.  The same systemic autoimmune disease provokes arthritis and endocarditis via distinct mechanisms.

Authors:  Bryce A Binstadt; Jennifer L Hebert; Adriana Ortiz-Lopez; Roderick Bronson; Christophe Benoist; Diane Mathis
Journal:  Proc Natl Acad Sci U S A       Date:  2009-09-15       Impact factor: 11.205

Review 5.  Group A Streptococcus, Acute Rheumatic Fever and Rheumatic Heart Disease: Epidemiology and Clinical Considerations.

Authors:  Liesl J Zühlke; Andrea Beaton; Mark E Engel; Christopher T Hugo-Hamman; Ganesan Karthikeyan; Judith M Katzenellenbogen; Ntobeko Ntusi; Anna P Ralph; Anita Saxena; Pierre R Smeesters; David Watkins; Peter Zilla; Jonathan Carapetis
Journal:  Curr Treat Options Cardiovasc Med       Date:  2017-02

Review 6.  Cardiac phenotype in mouse models of systemic autoimmunity.

Authors:  Chandan Sanghera; Lok Man Wong; Mona Panahi; Amalia Sintou; Muneer Hasham; Susanne Sattler
Journal:  Dis Model Mech       Date:  2019-03-08       Impact factor: 5.758

  6 in total

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