Cryostat sections of endomyocardial biopsies from 53 patients (mean age 41 +/- 5 years, 38 male and 15 female) clinically indicated to suffer from myocarditis were stained using monoclonal antibodies against subpopulations of T-lymphocytes and macrophages and with polyclonal rabbit-anti-human sera marking two calcium-binding proteins expressed by monocytes and macrophages appearing in inflammatory sites only. No inflammatory infiltrate cells were found in 13 cases (25%). Mononuclear cell infiltrates were present in 40 cases (75%). Ten biopsies showed a predominance of macrophages bearing the marker 27E10, characteristic for an early acute inflammation and 18 biopsies contained 25F9 positive macrophages, characteristic for a late stage of inflammation. An intermediate type of inflammation with both macrophage types present was found in 12 patients. Patients with immunohistologically confirmed myocarditis had atrial, ventricular or combined forms of arrhythmias (78%), scars in the vectorcardiogram (100%) and radiological evidence of cardiomegaly (36%). In conclusion, typing and endomyocardial biopsies for macrophage subpopulations is a sensitive new approach to assess the diagnosis of myocarditis.
Forty-one endomyocardial biopsies of the right interventricular septum have been investigated in 24 immunosuppressed patients after orthotopic heart transplantation. Monoclonal antibodies 27E10, 25F9, and RM3/1, which react with different macrophage phenotypes, and antisera MRP-8 and MRP-14, specific for proteins expressed on endothelial and monocyte cell surfaces in inflammation as well as markers for CD4+ and CD8+ T-lymphocytes, were employed in an indirect immunoperoxidase staining technique. This methodology permits more physiological recognition of the inflammatory process within the myocardium. It was possible to verify and to distinguish acute early, late and down-regulatory stages of inflammation in 33 biopsies (80%). No evidence of inflammation was found in seven biopsies (17%). Conventional histopathology with haematoxylin-eosin and Masson's trichrome was performed simultaneously, and demonstrated inflammation to be present in 23 of 41 biopsies (56%). An important findings is that CD4+ and CD8+ lymphocytes were absent in 15 of 41 specimens (37%) although there was inflammation proven by the presence of different macrophage phenotypes. The results indicate the necessity of long-term serial investigations of the physiological role of specific inflammatory macrophage phenotypes during the rejection process. It is concluded that the phenotyping of macrophage and endothelial cell differentiation antigens offers a sensitive approach to assess diagnosis of myocardial inflammation as a consequence of ongoing rejection in cardiac allografts.
In 14 patients [9 with loosened total hip arthroplasty (THA), 5 with primary osteoarthritis], the inflammatory cell infiltrate was characterized in cryostat tissue sections using antibodies against subsets of macrophages and lymphocytes. In all patients the abundance of a mature type macrophage (25F9+) was observed, whereas 27E10+ macrophages, characteristic of acute inflammatory reactions, were not seen in primary osteoarthritis but were found in 4 out of 9 patients with THA loosening. The RM3/1 + macrophage phenotype was seen in some of both sets of patients (osteoarthritis 4/5; THA loosening 4/9). The markers MRP8 and MRP14 typical of immature macrophages, were found in all patients with osteoarthritis and in some (4/9 and 8/9 respectively) of those with THA loosening. IOT4+ T-helper cells were only present in 1/5 5 patients with osteoarthritis and in 2/9 patients with THA loosening. IOT8+ T-suppressor lymphocytes were more frequently present (in 4/5 and 5/9 respectively). The data reveal remarkable differences between the two groups of patients. While the inflammatory infiltrate in patients with osteoarthritis lacks the characteristics of acute inflammation, in patients THA loosening the inflammatory process seems to be determined by periods of acute reactions. The occasional presence particularly of T-helper cells suggests that the inflammatory process is less T-cell but rather macrophage-driven.
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