Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Individuals with scabies react to bites by generating a cell-mediated immune response at the bite site. This elicits a very itchy papule that is often excoriated. Sometimes ulcerated papules, vasculitis, and nodules develop as a result of other immunologic reactions in skin. Immunologic reactions mediated by antibodies of the immunoglobulin G (IgG), IgM, and especially, IgE classes may also be involved. None of these reactions have been shown to eliminate all mites from the skin surface, but locally these reactions may prevent the epidemic multiplication of scabies' organisms on the skin surface, as observed in some patients with crusted scabies.
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PMID:The immunology of scabies. 847 30

Fifteen sural nerve biopsies of vasculitic neuropathies have been compared with 11 cases of different non-vasculitic neuropathies and normal nerves from brain-dead organ donors. The APAAP (alkaline phosphatase monoclonal anti-alkaline phosphatase) immunostaining method was applied to cryostat sections from unfixed snap-frozen tissue samples. Immunoglobulins IgG, IgM, IgA, complement factors and light chains were reactive in biopsies of normal nerves as well as of vasculitic and nonvasculitic neuropathies. A strong reaction against IgE in the epineurial vessel walls was only seen in cases of Churg-Strauss-vasculitis. Antibodies against MHC class II (HLA DR) were positive in most of vasculitic infiltrates. Vascular endothelial cells were positive with anti MHC class I in all biopsies. A typical finding in all vasculitic neuropathies was the infiltration of epineurial vessels with CD4 positive and, to a lesser extent, CD8 positive lymphocytes. CD22 positive lymphocytes (B cells) have only been seen in about one third of vasculitic neuropathies. CD16 positive cells (NK-cells or neutrophils) could be demonstrated only in two biopsies. CD68 positive cells (macrophages) are frequently seen in most cases of neuropathy regardless of their etiology. The results support the concept of a primary T-cell mediated process against epineurial vessels as the most important mechanism in the pathogenesis of vasculitic neuropathies. In some cases with small epineurial infiltrates the vasculitic process can only be recognized with antibodies against CD4 or CD8. Therefore, the immunohistochemical evaluation of sural nerve biopsies may be helpful for identifying cases with microvasculitis.
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PMID:Immunohistochemical findings in vasculitic neuropathies. 850 63

An 81-year-old man presented with a generalized maculopapular rash, lymphadenopathy, conjunctivitis and arthritis. Vasculitis was confirmed by skin biopsy and by direct immunofluorescence, which showed perivascular C3 and granular IgM accumulation. Histology of an inguinal lymph node was diagnostic for angioimmunoblastic lymphadenopathy with dysproteinaemia (AILD), and this was confirmed by the finding of hypergammaglobulinaemia and elevated IgE levels. Immunohistology on a lymph node biopsy showed a T-helper cell (CD4) infiltrate expressing the interleukin (IL)-2 receptor alpha and beta chains. While receiving prednisone 100 mg/day, the patient developed new lesions, mimicking a relapse of vasculitis, which were subsequently shown to be necrotizing herpes zoster. Serum IL-2 and IL-6 levels were elevated. To our knowledge, this is the first report of simultaneous elevation of IL-2 and IL-6 in AILD: IL-2 may be involved in proliferation of the malignant cell clone, and IL-6 in the pathogenesis of both the vasculitis (via endothelial cell activation) and the hypergammaglobulinaemia.
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PMID:Necrotizing herpes zoster mimicking relapse of vasculitis in angioimmunoblastic lymphadenopathy with dysproteinaemia. 854 55

Allergic granulomatosis accompanied by angiitis (Churg-Strauss syndrome) constitutes an unusual disorder which is characterized clinically by bronchial asthma and hypereosinophilia, accompanied by systemic symptoms of histopathologically and by necrotizing vasculitis, extravascular granulomas and tissue infiltration by eosinophils. We report a case of a 4 year-old child presenting with acute pneumonia and deteriorated general condition. The biopsy of an inflammatory pseudotumor of the right anterior orbit revealed necrotizing vasculitis, extravascular epitheloid granuloma and eosinophilic tissue infiltration. These are characteristic changes of allergic granulomatous vasculitis (Churg-Strauss syndrome. Laboratory findings were characterized by blood eosinophilia, increased IgE value and the presence of antineutrophil cytoplasmic ant antibodies (p-ANCA). Local and systemic manifestations quickly regressed after parenteral application of corticosteroids. Two exacerbations of inflammatory pseudotumor occurred after reduction of the corticosteroid dosage. Systemic vasculitic syndromes are rare in childhood. Orbital manifestations in Churg-Strauss syndrome in childhood have never been reported.
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PMID:Inflammatory pseudotumor of the anterior orbit. A symptom in allergic granulomatous angiitis (Churg-Strauss syndrome). 856 41

In the Brown-Norway rat, mercuric chloride (HgCl2) induces an autoimmune syndrome characterized by high IgE levels. There is widespread necrotizing leukocytoclastic vasculitis involving lung, skin, mucous membranes, pancreas, liver, and gut, with tissue injury being most marked in the cecum. As in systemic vasculitis in man, there are neutrophils at the site of tissue injury and the animals develop anti-neutrophil cytoplasmic antibodies, which in the Brown-Norway rat are directed against myeloperoxidase. To determine whether neutrophils are involved in the pathogenesis of the vasculitis, we have used a monoclonal antibody that was reported to deplete neutrophils in other rat strains. Rats treated with HgCl2 received antibody by intravenous injection at various time points. Serial blood samples were taken for neutrophil counts and to assay for anti-myeloperoxidase and IgE antibodies. The guts of animals killed after antibody therapy were scored for vasculitic changes and neutrophils infiltrate. RP3 (but not the control antibody MAC6) was shown to bind to Brown-Norway rat neutrophils and to block glycogen-induced influx of neutrophils into the peritoneum. When given at peak disease, RP3 caused a dose-dependent reduction in tissue injury with a marked reduction in circulating blood neutrophil numbers and in tissue neutrophil infiltrate. RP3 treatment did not affect the rise in titer of IgE and anti-myeloperoxidase antibodies. The data presented demonstrate that in this model neutrophils are necessary for the induction of vasculitis and that the degree of vasculitis correlates with neutrophil number. To our knowledge, this study is the first to provide direct evidence for a role for neutrophils in vasculitis. We suggest that antibodies directed against neutrophils, especially if they deplete neutrophils, may be useful in the therapy of vasculitis in man.
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PMID:Role of neutrophils in the pathogenesis of experimental vasculitis. 868 65

Experimental sensitization by repeated intramuscular injection of Ascaris suum antigen (Ag-As) supplemented with Freund's incomplete and complete adjuvants was carried out in 50 BALB/c CrSl c male mice (sensitized group) for 24 weeks, and the results were compared with those in a control group of 25 mice. At the injection sites of the sensitized group, granulomatous angiitis with eosinophil infiltration was observed in all mice, and fibrinoid angiitis in only four. By light and electron microscopic examinations pulmonary granulomatous vasculitis with a few eosinophils was observed at a high frequency (80%) after 12 experimental weeks. Immunohistochemical examination revealed pulmonary vascular and perivascular infiltration of L3/T4 (CD4) positive cells, B cells, IgG and C3 positive cells in addition to activated macrophages, Thy-1 T cells, IgE positive cells, and IgM positive cells after 12 experimental weeks. There were significant increases in the eosinophil cell count of the peripheral blood, the hemagglutination titers of the sheep erythrocytes, IgE and IgM antibodies to Ag-As by ELISA and Western blotting after 8 experimental weeks. After 12 experimental weeks the IgG antibody to the Ag-As was low, but it increased significantly, and the sera showed multiple precipitation lines to the Ag-As by the Ouchterlony method. In conclusion, the pulmonary granulomatous vasculitis in this study is considered to consist of allergic reactions of type IV and probably type III based on type I.
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PMID:Experimental granulomatous vasculitis induced by sensitization with Ascaris suum antigen in mice. 880 96

Mercuric chloride (HgCl2) induces a T cell-dependent autoimmune syndrome in Brown-Norway (BN) rats characterized by a humoral response, tissue injury with an accumulation of CD8+ and CD4+ T cells, and an increase in tissue IL-4 mRNA and serum IgE suggesting Th2 cell activation. In other models of autoimmune disease, CD8+ cells act in both anti- and pro-inflammatory capacities, suggesting that functionally distinct CD8+ populations exist in vivo. The effect of treatment with OX8, a depleting anti-CD8 MoAb, on the initiation of HgCl2-induced autoimmunity was assessed in two experiments in a total of 20 BN rats, and compared with 20 animals treated with a control MoAb or PBS. OX8 significantly depleted peripheral blood CD8+ lymphocytes, had no effect on HgCl2-induced anti-collagen or myeloperoxidase antibodies, nor on the incidence or severity of caecal vasculitis. The severity of HgCl2-induced arthritis was significantly reduced in OX8-treated animals; median peak score reduced from 7.5 to 3.0 (experiment 1) and from 7.0 to 4 (experiment 2) (P = 0.009, Mann-Whitney U-test). OX8 treatment also exacerbated the early rise in HgCl2-induced IgE and induced a significant rise in plasma interferon-gamma (IFN-gamma), suggesting that CD8+ cells may have a regulatory influence on Th cell populations. These data provide direct evidence that CD8+ cells may act in a proinflammatory capacity in both this model of autoimmunity and the pathogenesis of inflammatory arthritis.
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PMID:Anti-CD8 treatment reduces the severity of inflammatory arthritis, but not vasculitis, in mercuric chloride-induced autoimmunity. 891 74

The administration of mercuric chloride (HgCl2), gold compounds, or D-penicillamine to Brown Norway (BN) rats causes a T helper (Th)2 cell-associated autoimmune syndrome characterized by the production of a number of autoantibodies, marked elevation of serum IgE concentration, and tissue injury in the form of a vasculitis and arthritis. We have recently shown that the same compounds in vitro sensitize BN rat peritoneal mast cells for IgE-triggered mediator release and interleukin-4 mRNA production. We wished to test the hypothesis that these agents influence mast cell function via an effect on intracellular reactive oxygen species (ROS) production/redox balance. Mast cells were obtained from BN rats by peritoneal washout. Incubation with HgCl2, gold compounds or D-penicillamine (the latter only in the presence of copper ions) led to the intracellular production of ROS as shown by the oxidative production of the fluorescent compound 2',7'-dichlorofluorescein. Mast cells were more sensitive than splenocytes to this effect. Direct oxidative stress (exposure to H2O2) produced a similar sensitization for mediator release to that caused by HgCl2. Inhibition of ROS formation by desferrioxamine or catalase diminished the enhancement of IgE-mediated serotonin release caused by HgCl2, as did replenishment of intracellular glutathione. 2-Mercaptoethanol exacerbated the toxicity of HgCl2, perhaps due to the formation of a lipophilic complex that enhanced HgCl2 uptake. Blocking of glutathione synthesis increased the toxicity of HgCl2, but also abolished any sensitizing effect on mediator release. These results support three main predictions of our hypothesis: (1) the compounds known to influence mast cell function all lead to the generation of ROS within the mast cell; (2) direct oxidative stress causes sensitization for mediator release by the mast cell; and (3) modulation of ROS production/redox balance within the mast cell modulates the effects of these compounds on mast cell function. The balance of oxidative/antioxidative influences may play an important role in the modulation of mast cell function, particularly in the context of chemically induced autoimmunity.
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PMID:Alterations in intracellular reactive oxygen species generation and redox potential modulate mast cell function. 902 32

A 54-year-old man had suffered from bronchial asthma, followed by numbness and muscle weakness of the extremities. He was admitted to our department in July, 1994, because of progression of the symptoms. On admission, neurological examination revealed muscle weakness with atrophy and sensory disturbance of multiple mononeuritic type. Blood tests revealed eosinophilia and an increase in rheumatoid factor, IgE levels and P-ANCA. A sural nerve biopsy showed necrotizing vasculitis and inflammation with eosinophil infiltration. The patient was diagnosed as having allergic granulomatous angitis,and treated with steroid pulse therapy without beneficial effect. Plasma exchange was performed twice, which resulted in remarkable improvement in motor and sensory disturbance. The present case suggests that plasma exchange has beneficial effects on severe cases with allergic granulomatous angitis.
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PMID:[A case of allergic granulomatous angitis with beneficial effects of plasma exchange]. 916 42

D-penicillamine (DP) and gold salts which are used as immune-modulating agents in the treatment of rheumatoid arthritis are known to be capable of causing autoimmune manifestations. Most autoimmune diseases in man are dominated by Th1-type responses, and one might presume that effective immunotherapy counteracts Th activity, perhaps by causing a shift to a Th2 response. The mechanism of action of gold and DP is not clear, but some clues may be obtained from their effects in animal models. DP, gold salts and mercuric chloride (HgCl2) are known to induce Th2-dominated autoimmune syndromes in genetically susceptible rodent strains, and we have demonstrated recently that HgCl2 up-regulates messenger RNA (mRNA) for IL-4 in the Brown Norway (BN) rat. In the BN rat HgCl2 treatment is also associated with the development of vasculitis, and anti-myeloperoxidase (MPO) antibodies are found in the serum. The present study examined and confirmed the hypothesis that, since gold and DP induce an autoimmune syndrome similar to HgCl2 in the BN rat, they may also induce vasculitis and an up-regulation in mRNA for IL-4. Tissue injury was assessed macroscopically and histologically on day 5 and day 15 after the start of injections with gold, DP or HgCl2, serum titres of IgE and presence of anti-MPO antibodies were determined using ELISA, and a semi-quantitative assay using reverse transcription-polymerase chain reaction was used to assay the level of mRNA for IL-4 in spleen and caecum. The relative degree of tissue injury reflected the potency of induction of IgE by the three agents (HgCl2 being most potent and DP least potent). The lesions were identical histologically, supporting the premise that the vasculitis is a manifestation of the autoimmune syndrome rather than non-specific HgCl2 toxicity. Both gold and DP induced less up-regulation of mRNA for IL-4 than HgCl2. HgCl2 (but not gold or DP) induced anti-MPO antibodies. It would be interesting to examine patients treated with gold and DP to see if there is evidence of a Th2-type response in those developing autoimmune complications, and whether or not the bias to a Th2 environment contributes to efficacy of treatment of the underlying disease.
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PMID:Gold and D-penicillamine induce vasculitis and up-regulate mRNA for IL-4 in the Brown Norway rat: support for a role for Th2 cell activity. 918 89


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