ANTIBODIES TO LAMININ AND IMMUNOHISTOCHEMICAL LOCALIZATION OF LAMINININ CHRONIC CHAGASIC CARDIOMYOPATHY - A REVIEW

Citation
J. Milei et al., ANTIBODIES TO LAMININ AND IMMUNOHISTOCHEMICAL LOCALIZATION OF LAMINININ CHRONIC CHAGASIC CARDIOMYOPATHY - A REVIEW, Molecular and cellular biochemistry, 129(2), 1993, pp. 161-170
Citations number
38
Categorie Soggetti
Biology
ISSN journal
03008177
Volume
129
Issue
2
Year of publication
1993
Pages
161 - 170
Database
ISI
SICI code
0300-8177(1993)129:2<161:ATLAIL>2.0.ZU;2-C
Abstract
Antibodies against laminin were determined by ELISA in forty six patie nts suffering from Chagas' disease and twenty healthy persons (control group). The patients were divided into three groups according to the severity of clinical, electrocardiographic and echocardiographic studi es. Histologic, ultrastructural and immunohistochemical studies were m ade of endomyocardial biopsy specimens from 10 of these patients with chronic Chagasic cardiomyopathy. Antibodies to laminin were detected i n 50% of the patients in each of the three groups. However analysis of the data did not allow us to determine any significant correlation am ong the severity of the different clinical and non-invasive studies an d the level of circulating antibodies to laminin. The highest titers o f antilaminin antibodies were detected in the group with severe cardio logical alterations (37% of the patients). Histological and electron m icroscopic observation of myocardial biopsies disclosed marked thicken ing of the basement membranes of the myocytes, endothelial cells and v ascular smooth muscle cells. Light (peroxidase-labeled antibodies) and electron (gold-conjugated antibody) microscopic immunohistochemical m ethods revealed a positive reaction for laminin in these thickened bas ement membranes. This thickening may develop as a consequence of: a) a n immunologic reaction which is triggered by the presence of a laminin -like molecule on the surfaces of T. cruzi amastigotes and trypomastig otes; b) an immunologic response to direct injury of basement membrane s causing some of their components to become antigenic; c) myocardial fibrosis, with synthesis of new connective tissue components, and d) a combination of the preceding factors. The relationship of these chang es to antilaminin antibodies remains unclear. From these results, it i s not possible to assure a physiopathogenic role for antibodies to lam inin in chronic Chagas' cardiomyopathy.