Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antibodies to erythrocytes of sheep and human serum albumin were formed in rabbits with alimentary atherosclerosis as intensively as in control. Trasilol failed to affect the antibody formation in normal animals, but sharply decreased the production of specific immunoglobulins (especially the 7S) in rabbits with experimental atherosclerosis. Thus, the action of the preparation is realized not by way of direct inhibition of functional activity of the lymphoid tissue cells, but by inhibiting the immunostimulating factor circulating in the blood in experimental atherosclerosis.
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PMID:[The effect of the polyvalent proteinase inhibitor, trasylol, on antibody formation under normal conditions and in experimental atherosclerosis]. 108 67

Cellular immunity may play a role in the pathogenesis of atherosclerosis. In this report the potential role of these cells in the formation of abdominal aortic aneurysms by immunohistochemistry was investigated. Aortic tissues from 32 patients were examined: 4 normal aortas, 6 aortas with occlusive atherosclerotic disease, 17 abdominal aortic aneurysms, and 5 inflammatory abdominal aneurysms. Using monoclonal anti-CD3 (T cells), anti-CD19 (B cells), anti-CD11c (macrophages), anti-CD4 (T helper cells), and anti-CD8 (T suppressor cells), several distinctions among these groups were found. The amount of inflammatory cell infiltrate was as follows: inflammatory aneurysms more than abdominal aortic aneurysms more than occlusive aortas more than normal aortas. CD3-positive T lymphocytes rarely were found in the adventitia of normal or occlusive aortas. In contrast, abdominal aortic aneurysms and inflammatory aneurysms exhibited most of the CD3-positive infiltrates in the adventitia. CD19-positive B lymphocytes were present mainly in the adventitia of all pathologic tissues. The CD4-positive:CD8-positive ratio was greater in abdominal aortic aneurysms and inflammatory aneurysms than in the other groups, both in the adventitia and in the media of the aortas. CD11c-positive macrophages were present throughout the diseased tissues, often surrounded by lymphoid aggregates; the greatest numbers of macrophages were found in the inflammatory aneurysm group. Our data suggests that the aneurysmal disease may progress from occlusive disease and is accompanied by an increase in chronic inflammatory cells as well as a redistribution of these cell types. Therefore it is suggested that aneurysmal disease may represent an immune-mediated event.
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PMID:Human abdominal aortic aneurysms. Immunophenotypic analysis suggesting an immune-mediated response. 170 Jun 20

22 nephrectomy specimens of renal allografts in chronic rejection after periods between 3 and 96 months, were studied immunohistologically. Various cell types in the arterial wall were characterized with antibodies specific against different cells of the mononuclear phagocyte system, against smooth muscle cells, and against differentiating lymphoid cells. In addition, the metabolism of lipoproteins was investigated using appropriate antibodies against several apolipoproteins. Subendothelial plaques of foam cells were found to consist of macrophages in foamy transformation. At the stage of intimal fibrosis the smooth muscle cells are more prominent. Lymphatic infiltration consists almost exclusively of T-lymphocytes. Apolipoprotein analysis reveals deposits of Apo A1, A2 and B1, most of them extracellular. According to these results, it is not only immunologic factors that are involved in arterial wall reactions during chronic transplant arteriopathy, but disorders of the lipoprotein metabolism--probably due to endothelial dysfunction--are also playing an important role like in atherosclerosis.
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PMID:Apolipoproteins and immunohistological differentiation of cells in the arterial wall of kidneys in transplant arteriopathy. Morphological parallels with atherosclerosis. 179 92

This review article attempts to present an overview of the occurrence and function of lipid storage and secretory organelles: the lamellar bodies. Morphologically these organelles vary considerably in size (100 nm to 2400 nm); they are surrounded by a membrane and contain multilamellar lipid membranes. Lamellar bodies may also contain apolipoproteins and lytic enzymes and have an acidic pH, which confers on them a lysosomal character. Under normal physiological conditions, the main function of lamellar bodies is the supply of extracellular domains with specialized lipid components related to a specialized function. The lamellar bodies of the lung epithelium are best investigated in their functional and structural features and are the storage form of the lung surfactant. They provide a monomolecular lipid film of dipalmitoyl phosphatidylcholine (DPPC) on the surface of lung alveoli to lower surface tension necessary for optimal gas exchange and a hydrophobic protective lining against environmental influences. Additional cells of the respiratory system such as the mucosa of the human nose and the bronchi contain lamellar bodies. Lamellar bodies are also found in the gastrointestinal tract, in tongue papillae, oral epithelium, and mucosa cells of the stomach. The major phospholipid of lamellar bodies in mucosa cells of the stomach is DPPC, providing a hydrophobic protective lipid film against the tissue-damaging activities of gastric juice. The hydrophobic water-protective barrier of the skin, which consists mainly of neutral lipids, however, also originates from lamellar bodies secreted by epithelial cells. Lamellar bodies, mainly consisting of DPPC, also occur in mesodermal cell layers of sliding surfaces to provide the lubrication of joints, of the peritoneum, pericardium, and pleural mesothelium. In certain pathological conditions, such as atherosclerosis, Niemann-Pick disease, lecithin:cholesterol acyltransferase (LCAT) deficiency, cholestasis, degeneration of nerves and brain, and regeneration of nerves and wound healing, lipid-containing lamellar bodies have been observed in various cells, the function of which still remains to be elucidated. In early and late lesions of atherosclerotic plaques, lamellar bodies, consisting of unesterified cholesterol and phospholipids, are associated with the extracellular matrix of the intima. During regression of fatty streaks, lamellar bodies are seen intracellularly in macrophages and smooth muscle cells. Inherited metabolic disorders, such as Niemann-Pick disease type I and type II, result in the excessive accumulation of lamellar body-containing cells, for example in bone marrow, spleen, and lymphoid tissue. Type I is a deficiency in sphingomyelinase and type II is a defect in intracellular trafficking of lipoprotein-derived cholesterol.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Structure and function of lamellar bodies, lipid-protein complexes involved in storage and secretion of cellular lipids. 179 38

Chronic rejection has several histological appearances, depending on the type of organ graft. Common to all of them is transplant arteriosclerosis associated with an ongoing inflammatory response in the transplanted graft. To the contrary of classical atherosclerosis, in which the manifestations are mostly focal, proximal, and asymmetric, transplant arteriosclerosis is generalized, and the intimal thickening is concentric. In this article, we describe an experimental animal model whereby transplant arteriosclerosis may be investigated in the inbred rat. Aortic allografts were transplanted from DA (RTIa) to major histocompatibility complex-incompatible WF (RTIv) rats or, for control, to rats of the DA strain. Transplantation was followed by an acute inflammation episode in the aortic adventitia of the allograft, largely lacking in the syngeneic graft, with a prominence of lymphoid activation markers (Cd25) in the cells of the inflammatory infiltrate. The inflammation episode peaked at 2 months after transplantation, became attenuated, and was followed by a proliferative response of myocytes in the allograft media. An increase in the migration of myocytes to the subendothelial space (presumably through small breaks generated in the internal elastic lamina) was observed thereafter, and myocyte proliferation continued in the intima with some intermingled macrophages. Finally, necrosis and disappearance of myocytes and their replacement by fibrous tissue were observed in the media. These alterations are virtually identical with the vascular lesion of chronically rejecting parenchymal organ transplants in human subjects. We suggest that aortic allografts exchanged between histoincompatible rat strains may be used as an experimental model for transplant arteriosclerosis.
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PMID:Chronic rejection in rat aortic allografts. An experimental model for transplant arteriosclerosis. 202 5

During repair of an inflammatory abdominal aortic aneurysm, fresh samples of the aneurysm wall were obtained. Histology confirmed the diagnosis of chronic periaortitis,- advanced atherosclerosis with medial attenuation, and periaortic inflammation. Monoclonal antibodies were used to identify the cells of the inflammatory infiltrate. The majority of the adventitial lymphocytes were B cells. No B cells were present in the atheroma. The majority of mature plasma cells contained IgG with a few plasma cells containing IgM. T cells, predominantly T helper cells, were found in the atheroma and adventitia. Positive DR staining was shown by the majority of lymphocytes, by macrophage-like cells in germinal centers of lymphoid follicles in the adventitia, by some vascular endothelial cells, and by some smooth muscle cells. The implications of these findings are discussed.
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PMID:Characterization of inflammatory cells in a patient with chronic periaortitis. 226 85

For a historical survey of the pathogenesis of atherosclerosis the reader is referred to references 1 and 2. Comprehension of the vessel-blood interface homeostasis hinges upon an understanding of the pathophysiology of angio-lymphoid relationships. Even in the smooth contact of the intact hydrophobic intimal lining with the marginal flow of the circulatory stream, small amounts of thrombin and small aggregates of aging platelets float by under physiologic conditions. Since endothelial cells of the vascular intima contain receptors for thrombin, filling these receptors with thrombin becomes a stimulus for the production of prostacyclin (PGI2) by the endothelial cells; PGI2 in turn inhibits adherence of the small platelet aggregates by ADP; homeostasis is maintained. The size of physiologic thrombin-producing platelet microaggregates is controlled by physiologic levels of antithrombin III.
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PMID:Atherosclerosis. I. A leiomyoproliferative disease of the arteries resulting from breakdown of the endothelial barrier to potent blood growth factors. II. Perspectives in atheroprophylaxis. 299 35

A total of 145 BB Wistar diabetic rats, 46 of their nondiabetic siblings, and 43 outbred Wistar rats were autopsied and the frequency of lesions in all organ systems were determined. Common strain-related lesions included pulmonary infections, granulomas, lymphoid hyperplasia, lymphomas, lymphocytopenia, eosinophilia, supradiaphragmatic accessory lobes of the liver, and prostatic atrophy. These suggest some basic strain-related abnormalities of the immune system that were selected by the process of inbreeding. Diabetes-related lesions were insulitis, testicular atrophy, cataracts, hepatic fatty change, pancreatitis, lymphocytic thyroiditis, hypoglycemic brain damage, central pontine myelinolysis, stomach erosions, and idiopathic megacolon. Many of these are sequelae of human juvenile-onset diabetes and support the validity of the BB Wistar rat as an animal model for human diabetes mellitus. The absence of several important sequelae of the human disease (i.e., diabetic nephropathy, atherosclerosis, and severe microangiopathy) suggests a degree of infidelity as a model for human diabetes mellitus. Nonspecific lesions occurring in all three groups of rats included myocardial degeneration and fibrosis, splenic extramedullary hematopoiesis, and chronic progressive glomerulonephropathy.
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PMID:Pathological lesions in the spontaneously diabetic BB Wistar rat: a comprehensive autopsy study. 634 94

We studied the antigenic markers of macrophages (Mphs) in atherosclerotic human arteries by immunohistochemistry and compared them with the patterns in Mph subpopulations of tonsil and lymph node, which are also described. The staining of atheroma intimal Mphs was assessed semiquantitatively in the subendothelial, mid, and outer intima. Three patterns of reactivity with Mph antibodies were recognized. (a) Pan-Mph (antibodies HAM56, EBM11, and CD14 group). Staining was maximal in the mid-intimal zone. (b) Subendothelial Mphs (anti-muramidase, anti-alpha-1-antitrypsin and MAC387). In lymphoid tissue, sinusoidal Mphs and a few inflammatory Mphs were stained, as well as blood monocytes. This group of antibodies recognizes Mphs that are likely to be recently blood-derived (RBD-Mphs). (c) Antibodies reactive with various histiocyte populations in lymphoid tissues (anti-Factor XIII; anti-HLA Class II and LN2) also gave maximal staining in the mid-intimal zone, but differences between lesion types suggest that they are recognizing heterogeneous subpopulations of Mphs. These observations demonstrate the heterogeneity of tissue Mphs and suggest that an insight into the dynamics of tissue Mphs can be obtained from the cell phenotype. They indicate that all stages of atherosclerosis can have an outward traffic of Mphs from the blood through the arterial intima.
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PMID:The immunohistochemical heterogeneity of atheroma macrophages: comparison with lymphoid tissues suggests that recently blood-derived macrophages can be distinguished from longer-resident cells. 750 8

The expression of PECAM, ICAM-1, VCAM-1, and E-selectin was studied in 64 samples of human coronary arteries taken from 15 explanted hearts obtained within 5 min of transplantation. Normal artery (n = 12), predominantly fibrous plaques (n = 23), and plaques containing extracellular lipid (n = 26) and three segments showing recanalization channels were studied. All endothelial cells strongly and equally expressed PECAM; positive staining was used to check that artefactual denudation of the endothelial surface had not occurred. PECAM was also present in some lipid-filled macrophages. Normal arteries showed no VCAM-1 staining but focal segments of the endothelium were positive for ICAM-1 and E-selectin. ICAM-1 was strongly and constantly expressed by the endothelium over all types of plaques and in macrophages. E-selectin expression was confined to endothelial cells and occurred on the surface in 35 per cent of fibrous and 22 per cent of lipid-containing plaques. VCAM-1 staining of surface endothelium occurred in 39 per cent of fibrous and 20 per cent of lipid-containing plaques. A population of spindle-shaped cells of macrophage type (positive for EMB11 antigen) expressed VCAM-1 in lipid-containing plaques. Adventitial vessels adjacent to plaques showed endothelial expression of ICAM-1 and E-selectin. VCAM-1 staining of adventitial vessel endothelium was associated with local lymphoid aggregation. In conclusion, the expression of cell adhesion molecules is an important element in the inflammatory component of atherosclerosis and contributes to both monocyte and lymphocyte activation and recruitment from adventitial vessels and the arterial lumen.
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PMID:The expression of the adhesion molecules ICAM-1, VCAM-1, PECAM, and E-selectin in human atherosclerosis. 750 7


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