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Query: UMLS:C0042384 (vasculitis)
20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The human vasculitides including Takayasu's arteritis are idiopathic syndromes for which both autoimmune and infectious etiologies have been proposed. Although proof of a correlation between infection and human vasculitis would aid in patient management, it is difficult to confirm causality. To study infection-mediated vascular disease, different animal models have been developed. Infections with the bacteria C. pneumoniae, an RNA virus, and herpesviruses all cause vascular pathology and will be reviewed here. Many aspects of the human diseases are recapitulated in these models, so further animal studies may help elucidate mechanisms of infection-mediated vasculitis. Such results may improve management, and potentially, prevention of these important human diseases. Importantly, the animal models provide an opportunity to define how the immune and inflammatory processes function in the great vessels and the molecular basis for the selectivity of certain viral infections for the great elastic arteries.
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PMID:Animal models of infection-mediated vasculitis: implications for human disease. 1098 Mar 35

Infection of medial smooth muscle cells with gamma-herpesvirus 68 (gammaHV68) causes severe chronic vasculitis that is restricted to the great elastic arteries. We show here that persistence of disease in the great elastic arteries is (a) due to inefficient clearance of viral infection from this site compared with other organs or other vascular sites, and (b) associated with failure of T cells and macrophages to enter the virus-infected elastic media. These findings demonstrate immunoprivilege of the media of the great elastic arteries. We found that IFN-gamma acted on somatic cells during acute infection to prevent the establishment of medial infection and on hematopoietic cells to determine the severity of disease in this site. The immunoprivileged elastic media may provide a site for persistence of pathogens or self antigens leading to chronic vascular disease, a process regulated by IFN-gamma actions on both somatic and hematopoietic cells. These concepts have significant implications for understanding immune responses contributing to or controlling chronic inflammatory diseases of the great vessels.
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PMID:IFN-gamma action in the media of the great elastic arteries, a novel immunoprivileged site. 1116 Jan 43

Superantigens have been suggested to play an important role in the pathogenesis of several inflammatory skin diseases as well as systemic diseases such as atopic dermatitis, psoriasis, vasculitis, T-cell lymphoma and autoimmune diseases. Infections often precede the onset and relapse of these diseases, and antibiotic treatment with or without additional glucocorticosteroids and immunoglobulins is occasionally successful. Superantigens are microbial proteins that are able to stimulate up to 20% of the naive T-cell population in a non-specific way. They are produced by gram-positive and -negative bacteria as well as by viruses, parasites and yeasts. The importance of the pathogenic role of superantigens is determined by the potency to induce inflammation by extensive cytokine release after T-cell stimulation and/or T-cell-mediated cytotoxicity and, thereby, tissue damage. Furthermore, superantigens may be able to induce autoimmune processes by stimulation of autoreactive T-cells as well as autoantibody production by stimulation of B-cells. Among the diseases associated with superantigens, atopic dermatitis, guttate and chronic plaque psoriasis, as well as Kawasaki disease, are by far the best-characterized. Nevertheless, conflicting results have been obtained and formal proof of a pathogenic role of superantigens in these diseases is still lacking. The aim of this review is to summarize the data on superantigens in terms of their distribution in microorganisms, their interactions with the adaptive immune system and their contribution to skin pathology.
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PMID:Superantigens and their association with dermatological inflammatory diseases: facts and hypotheses. 1120 Aug 27

Infection with a newly described endotheliotropic adenovirus was the cause of a 1993 epizootic reminiscent of hemorrhagic disease in California mule deer (Odocoileus hemionus columbianus and O. hemionus hemionus). Pulmonary edema and intestinal luminal hemorrhage, or necrotizing stomatitis associated with systemic or localized vasculitis, respectively, were common lesions seen in animals that died during the epizootic. In order to determine if white-tailed deer (Odocoileus virginianus) also are susceptible to infection and fatal disease with the deer adenovirus, eight white-tailed deer fawns (4- to 6-mo-old) were inoculated with purified deer adenovirus. Four were inoculated intravenously and four were inoculated through the mucous membranes. Seven days post-inoculation, one of the fawns inoculated intravenously died. Pulmonary edema and hemorrhagic enteropathy were associated with pulmonary and intestinal vasculitis with systemic multiorgan distribution of endotheliotropic adenovirus as demonstrated by transmission electron microscopy and immunohistochemistry. Adenovirus was reisolated from lung homogenates of the fawn that died of adenovirus hemorrhagic disease.
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PMID:Experimental adenovirus hemorrhagic disease in white-tailed deer fawns. 1127 90

Infection with Trypanosoma cruzi causes a generalised vasculitis of several vascular beds. This vasculopathy is manifested by vasospasm, reduced blood flow, focal ischaemia, platelet thrombi, increased platelet aggregation and elevated plasma levels of thromboxane A(2) and endothelin-1. In the myocardium of infected mice, myonecrosis and a vasculitis of the aorta, coronary artery, smaller myocardial vessels and the endocardial endothelium are observed. Immunohistochemistry studies employing anti-endothelin-1 antibody revealed increased expression of endothelin-1, most intense in the endocardial and vascular endothelium. Elevated levels of mRNA for prepro endothelin-1, endothelin converting enzyme and endothelin-1 were observed in the infected myocardium. When T. cruzi-infected mice were treated with phosphoramidon, an inhibitor of endothelin converting enzyme, there was a decrease in heart size and severity of pathology. Mitogen-activated protein kinases and the transcription factor activator-protein-1 regulate the expression of endothelin-1. Therefore, we examined the activation of mitogen-activated protein kinases in the myocardium by T. cruzi. Western blot demonstrated an extracellular signal regulated kinase. In addition, the activator-protein-1 DNA binding activity, as determined by electrophoretic mobility shift assay, was increased. Increased expression of cyclins A and cyclin D1 was observed in the myocardium, and immunohistochemistry studies revealed that interstitial cells and vascular and endocardial endothelial cells stained intensely with antibodies to these cyclins. These data demonstrate that T. cruzi infection of the myocardium activates extracellular signal regulated kinase, activator-protein-1, endothelin-1, and cyclins. The activation of these pathways is likely to contribute to the pathogenesis of chagasic heart disease. These experimental observations suggest that the vasculature plays a role in the pathogenesis of chagasic cardiomyopathy. Additionally, the identification of these pathways provides possible targets for therapeutic interventions to ameliorate or prevent the development of cardiomyopathy during T. cruzi infection.
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PMID:The role of endothelin in the pathogenesis of Chagas' disease. 1133 35

We reported the case of a 39-year-old man with dermatomyositis (DM) complicated with subcutaneous emphysema and pneumomediastinum during steroid therapy. The patient had complained of muscle weakness, dyspnea and skin eruption on his anterior chest wall 6 months prior to admission. He was diagnosed as having DM on the basis of an elevation in myogenic enzymes, myogenic changes in electromyography, a skin biopsy and a muscle biopsy. Chest roentgenogram revealed interstitial pneumonia (IP) in the lower lobes of the lungs. The administration of prednisolone (60 mg/day) was initiated, which resulted in improvement of DM. Fifteen days after the initiation of the steroid therapy, the patient developed subcutaneous emphysema and pneumomediastinum. Additional administration of cyclosporin A (CsA) enabled us to rapidly taper the dose of prednisolone without aggravating the diseases. Several reports have shown that vasculitis might be involved in the pathogenesis of pneumomediastinum in DM patients. Infection and tissue fragility due to steroid therapy worsen the outcome of those patients. CsA therapy may improve the outcome through the anti-vasculitic- and steroid sparing-effects.
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PMID:[A case of dermatomyositis complicated with pneumomediastinum that was successfully treated with cyclosporin A]. 1150 15

Chronic hepatitis C virus (HCV) infection is frequently associated with a variety of autoimmune phenomenons. Mixed cryoglobulinemia (MC) appears in up to 50% of chronic HCV-infected patients. Cryoglobulins consist of immunoglobulin complexes precipitating in vitro when cooled below body temperature. In most cases IgM with rheumatoid factor activity is found in cryoprecipitates which could lead to vasculitis induced by the deposition of immnuocomplexes in small vessels. This vasculitis is thought to cause clinical symptoms called Meltzer's triad. This triad is represented by purpura, arthralgia and weakness. One third of patients suffering from HCV-associated mixed cryoglobulinemia are developing typical symptoms during their course of disease. The striking association between HCV infection and MC has conduced to the hypothesis that HCV is of major importance in the production of MC with followed vasculitis. Both hepatrophism and lymphotrophism have been reported for the hepatitis C virus. Infection of B-cells by HCV could probably lead to a bcl-2 translocation and immunoglobulin gene rearrangement which results in clonal lymphoproliferation and in synthesis of monoclonal IgM with rheumatoid factor activity. These IgM form immunocomplexes with IgG in the cold, which are finally responsible for the described vasculitis. Histopathological changes of the liver are dominated by chronic HCV infection. The majority of times mild activity of hepatitis or mild fibrosis could be found. Nevertheless, cirrhosis is more often found in HCV-infected patients suffering from MC compared to patients without MC. Conventional treatment of MC is aimed to reduce circulating immune complexes by immunosupression and plasmapheresis. With the emerging concept of a viral pathogenesis the therapeutic approach has changed during the last decade. Interferon treatment of MC, particularly of HCV-associated MC is well established nowadays.
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PMID:Hepatitis C virus-associated mixed cryoglobulinemia. Clinical manifestations, histopathological changes, mechanisms of cryoprecipitation and options of treatment. 1164 46

Leucocytoclastic vasculitis is a small vessel inflammatory disease mediated mostly by deposition of immune complexes. Infections, medications, chemicals, bacteria, viruses, and diseases associated with immune complexes have been accused in the pathogenesis. Cutaneous leucocytoclastic vasculitis presents as palpable purpura most often localized in the lower extremities, often accompanied by abdominal pain, arthralgia and renal involvement. The clinical diagnosis of leucocytoclastic vasculitis is confirmed histopathologically by skin biopsy. In order to determine the cause of the disease, depending on the patient's history, complete blood cell count, blood cultures, cryoglobulins, serum protein electrophoresis, rheumatoid factor, antinuclear antibody, and autoantibodies to neutrophilic cytoplasmic antigens and complement should be checked. Once the diagnosis of leucocytoclastic vasculitis is made, emphasis should be on the search for an etiological factor and the identification of the involved organs. If possible, the underlying cause should be treated or removed, for example discontinuation of drugs. The prognosis depends on the disease that has the cutaneous leucocytoclastic angiitis as a component, as well as the severity of internal organ involvement. For example, a patient with cutaneous leucocytoclastic angiitis and moderate nephritis as component of Henoch-Schonlein purpura has a much better prognosis than a patient with these same findings as a component of Wegener's granulomatosis. Only if physicians recognize and report severe reactions to regulatory authorities and manufacturers, new drugs associated with a risk of such reactions can be identified.
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PMID:Leucocytoclastic vasculitis: an update for the clinician. 1184 48

In 1998, an outbreak of acute encephalitis with high mortality rates among pig handlers in Malaysia led to the discovery of a novel paramyxovirus named Nipah virus. A multidisciplinary investigation that included epidemiology, microbiology, molecular biology, and pathology was pivotal in the discovery of this new human infection. Clinical and autopsy findings were derived from a series of 32 fatal human cases of Nipah virus infection. Diagnosis was established in all cases by a combination of immunohistochemistry (IHC) and serology. Routine histological stains, IHC, and electron microscopy were used to examine autopsy tissues. The main histopathological findings included a systemic vasculitis with extensive thrombosis and parenchymal necrosis, particularly in the central nervous system. Endothelial cell damage, necrosis, and syncytial giant cell formation were seen in affected vessels. Characteristic viral inclusions were seen by light and electron microscopy. IHC analysis showed widespread presence of Nipah virus antigens in endothelial and smooth muscle cells of blood vessels. Abundant viral antigens were also seen in various parenchymal cells, particularly in neurons. Infection of endothelial cells and neurons as well as vasculitis and thrombosis seem to be critical to the pathogenesis of this new human disease.
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PMID:Nipah virus infection: pathology and pathogenesis of an emerging paramyxoviral zoonosis. 1246 31

Vasculitides are a heterogeneous group of syndromes characterized by inflammation of the vessel wall. Several microbial pathogens have been known or suspected to cause vasculitis, and the development of molecular biology has promoted the search and confirmation of infectious agents in idiopathic vasculitis. Though several agents present primarily as an infectious process with vasculitis as an occasional manifestation, vasculitis may be the major manifestation of disease. Less definitive, and more controversial, is the role of infection and inflammation of the vessel wall in the pathogenesis of atherosclerotic disease. Clinical features can be nonspecific, and a high index of suspicion is required in order to make a diagnosis of vasculitis. Infection should always be excluded based on appropriate cultures and serologic assays, and, if confirmed, early and aggressive treatment should be instituted. However, in many instances, especially if there is a delay in the diagnosis, surgical intervention becomes necessary to treat the associated anatomic and physiologic sequelae.
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PMID:Infectious etiology of vasculitis: diagnosis and management. 1262 44


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