Immunohistochemical characterization of the lesions of canine idiopathic pericarditis

Pericardial tissue was obtained from 14 dogs with idiopathic pericarditis, and from three dogs with pericardial effusion associated with neoplastic disease, for histopathological assessment and characterisation of infiltrating leucocytes by immunohistochemistry. The major pathological change was ext...

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Bibliographic Details
Published in:Journal of small animal practice 2002-09, Vol.43 (9), p.382-387
Main Authors: Day, M.J, Martin, M.W.S
Format: Article
Language:English
Subjects:
Animals
Antibody Formation
complement
Dog Diseases - immunology
Dog Diseases - pathology
Dogs
Female
fibrosis
immune response
immunoglobulin G
immunohistochemistry
inflammation
macrophages
major histocompatibility complex
Male
pathogenesis
pericardial effusion
pericarditis
Pericarditis - immunology
Pericarditis - pathology
Pericarditis - veterinary
pericardium
plasma cells
T-lymphocytes
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Description
Summary:Pericardial tissue was obtained from 14 dogs with idiopathic pericarditis, and from three dogs with pericardial effusion associated with neoplastic disease, for histopathological assessment and characterisation of infiltrating leucocytes by immunohistochemistry. The major pathological change was extensive pericardial fibrosis which was generally accompanied by a mixed inflammatory response that was of greatest intensity at the cardiac surface of the tissue. Perivascular lymphoplasmacytic aggregates were present at the pleural surface and within the fibrosed pericardium. There were no features that clearly distinguished the samples from dogs with neoplastic disease from dogs with idiopathic pericarditis. The pericardial infiltrates were dominated by MAC 387+ monocyte-macrophages and plasma cells expressing immunoglobulin (Ig)A or IgG. CD3+ T lymphocytes and major histocompatibility complex (MHC) class II+ macrophages were less common, although the perivascular aggregates were mixtures of T and B lymphocytes and a proportion of fibroblasts expressed MHC class II. There was no vascular pathology or deposition of immunoglobulin or complement within vessel walls. These findings are consistent with an immune response dominated by humoral effector mechanisms (Th2 immunity) but do not clearly support a primary immune-mediated pathogenesis for idiopathic pericarditis.
ISSN:0022-4510
1748-5827
DOI:10.1111/j.1748-5827.2002.tb00088.x