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)

A patient with cutaneous vasculitis during infective endocarditis due to Lactobacillus casei was studied. Immune complexes (IC) were isolated from serum at the time of diagnosis and after 4 wk of therapy. Purification of IC used differential polyethylene glycol precipitation and competitive binding to staphylococcal protein A. In situ radioiodination of IC was performed, followed by SDS-polyacrylamide gel electrophoresis (PAGE). Anti-IC antisera were raised in rabbits by immunization with purified IC. IC were characterized by SDS-PAGE followed by electrophoretic transfer to nitrocellulose, incubation with antiserum and then with 125I protein A, and autoradiography. Although early and late IC differed quantitatively, there were no differentiating immunochemical features. Both IC contained a 60,000 dalton component that did not react with preimmune serum nor with anti-normal human serum. This component reacted with antiserum rendered specific for L. casei by affinity chromatography. The restricted antigen-antibody representation in IC contrasted with a wider panel of antibody activity in patient serum. The Western blot analysis proves to be an ideal method for the characterization of IC because of its sensitivity, dissociative capability, and preservation of immunoreactivity. IC isolated at a time removed from the original antigenic challenge may provide insight into the nature of the inciting antigen.
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PMID:Characterization of sequential immune complexes in infective endocarditis by Western blot analysis. 642 35

S antigen was isolated from human and bovine retinas and purified by two chromatographic steps. Its purity was controlled by SDS-electrophoresis and immunodiffusion. Seven Cynomolgus monkeys received a single subcutaneous immunization with either 50 or 100 micrograms of human S antigen (5 animals) or 100 micrograms of bovine S antigen (2 animals) with complete Freund's adjuvant. All the monkeys had bilateral uveoretinitis and anti-"S" antibodies were found in their serum. The time course of the disease was followed clinically during one year and pathologic features were described at various time intervals. The disease includes prominent retinal vasculitis and granulomatous chorio-retinitis, with a chronic course, and leads after many months to almost complete destruction of the retina, with persistence of inflammatory infiltrates and pigment of cell migration.
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PMID:[Experimental uveoretinitis induced in monkeys by retinal S antigen. Induction, histopathology (author's transl)]. 729 63

Angiogenesis is an important process in chronic inflammatory diseases. We observed that sera from patients with systemic vasculitis stimulated angiogenesis in an in vitro model using human umbilical vein endothelial cells cultured on a basement membrane (Matrigel) substrate. After 40% ammonium sulfate precipitation, angiogenic activity remained in the low molecular weight fraction and could be inactivated by heat. SDS-page of serum FPLC fractions exhibiting maximal angiogenic activity demonstrated two prominent species of 45 and 16-20 kD in patients' sera. These bands were much less apparent in sera obtained from control subjects. Amino-terminal sequencing of the 45-kD protein demonstrated that it was haptoglobin. Purified haptoglobin stimulated angiogenesis in a dose-dependent manner. The angiogenic activity of vasculitis patients' sera was partially inhibited by an antihaptoglobin antibody. Furthermore, serum haptoglobin levels in vasculitis patients correlated both with disease and angiogenic activity. Haptoglobin angiogenic activity was confirmed in two in vivo models using an implanted disc and a subcutaneous injection of basement membrane. Stimulation of angiogenesis is a newly recognized biological function of haptoglobin. The increased levels of haptoglobin found in chronic inflammatory conditions may play an important role in tissue repair. In systemic vasculitis, haptoglobin might also compensate for ischemia by promoting development of collateral vessels.
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PMID:Identification of haptoglobin as an angiogenic factor in sera from patients with systemic vasculitis. 768 Jun 72

The central features of Kawasaki disease are immune activation and cytokine-mediated generalized vasculitis. To identify the predisposing factors, we examined the antibody response to BCG antigens, since reactivation of a previous BCG inoculation site is an early, specific manifestation of this disease. BCG antigens were separated on SDS-PAGE, transferred to membrane, and incubated with acute- and convalescent-phase sera of 21 patients with Kawasaki disease. Sera were also examined for the presence of antibodies to mycobacterial 65-kDa heat-shock protein (HSP65), and to its human homolog P1 antigen using synthetic peptides of nonhomologous region. To demonstrate the HSP65-sensitized T cells, in vitro proliferation assay was performed. All convalescent, but not acute phase, sera showed a strong antibody reactivity against 65-kDa protein. The reactivity was directed to recombinant HSP65. Non-cross-reactive sequences between rHSP65 and human HSP65 cognate were synthesized. The sera recognized these peptides of rHSP65 and autologous P1 antigen. Peripheral lymphocytes proliferated following the addition of rHSP65 (stimulation indices, 2.16-7.82; mean, 4.54). These findings suggest that HSP65 may be the most potent factor predisposing to Kawasaki disease, and that an autoreactivity to the epitope of the human HSP65 homolog may be related to the susceptibility to the disease.
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PMID:Presence in Kawasaki disease of antibodies to mycobacterial heat-shock protein HSP65 and autoantibodies to epitopes of human HSP65 cognate antigen. 768 92

Chronic hepatitis C virus infection can be associated with mixed cryoglobulinemia and systemic vasculitis. The pathogenesis remains poorly understood. 55 consecutive patients with chronic HCI infection (anti-HCV- and serum HCV RNA-positive) were studies prospectively. Cryoglobulinemia was detected in 28 patients (51%) with a mean cryocrit level of 2.2%. Clinical symptoms of vasculitis were encountered in six patients. Compared to those HCV-infected patients without cryoglobulinemia the following distinctive features were observed in the presence of cryoglobulinemia: increased age (p<0.02), female preponderance (p<0.002), longer-lasting HCV infection (mean of 10.7 vs. 4.7 yrs), higher prevalence of cirrhosis (42.8 vs. 0%), increased serum concentration of IgM and increased rheumatoid factor activity, decreased concentration of serum C4 (each p<0.05). The response to interferon treatment was similar in patients with and without cryoglobulinemia. When cryoprecipitates were analyzed by immunofixation, type II cryoglobulinemia was present in 1/3 and type III in 2/3 of patients. By SDS-PAGE four different proteins were demonstrable in cryoprecipitates each identified by immunoblotting as IgG and IgM heavy or light chains respectively. Cryoprecipitate IgGs were shown to react with HCV structural as well a non-structural proteins in a recombinant immunoblotting assay (RIBA). In contrast, cryoprecipitate IgMs reacted only to the HCV core protein c22-3. HCV RNA was detected in cryoprecipitates without a significant enrichment when compared to the corresponding serum or supernatant HCV RNA content. Given the monoclonality of some cryoprecipitate IgM and their reactivity to HCV core, a cross-reactivity to IgG was postulated. In fact, when performing a computer-assisted search for sequence homology, a motif within the core protein (EGLGWAGWL, conserved in HCV genotypes) was identified homologous to a sequence of IgG heavy chains. Thus, temperature-dependent affinity changes of IgM anti-HCV core (nonapeptide) and ensuing complex formation with IgG via binding to the homologous IgG sequence could be a mechanism of cryoprecipitate formation.
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PMID:Cryoglobulinemia in chronic hepatitis C virus infection: prevalence, clinical manifestations, response to interferon treatment and analysis of cryoprecipitates. 860 Jun 60

In this paper, we report the purification and partial characterization of human platelet aggregation factor form the extracellular products (ECP) of Streptococcus mitis (S. mitis) isolated from a patient with Kawasaki disease (KD). Platelet aggregation reaction was carried out using platelet-rich plasma (PRP) and washed platelets suspended in ACD-PBS. The aggregation factor was designated as S. mitis-derived human platelet aggregation factor (Sm-hPAF). The results obtained were as follows. 1) Sm-hPAF was isolated by chromatography on DEAE-Sepharose CL-6 B, hydroxyapatite and Superdex 75 columns. The purified Sm-hPAF showed a single band upon SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and molecular weight of approximately 66 kDa on SDS-PAGE. The isoelectric point (pI) of Sm-hPAF was 8.5, and Sm-hPAF showed an absorption peak at 278 nm on absorption spectra. When the platelet aggregation activity of the Sm-hPAF was compared with that of ECP, the specific aggregation activity of the of Sm-hPAF was significantly increased (up to 28-fold). Sugars were not found in Sm-hPAF. The sequence of the first 15 amino-terminal amino acid residues were H.Asp-Glu-Gln-Gly-Asn-Arg-Pro-Val-Glu-Thr-Glu-Asn-Ile-Ala-Arg. The platelet aggregation activity of Sm-hPAF was inactivated by heating at 45 degrees C for 10 min. 2) PGE2 was released from platelets after incubation for 10 min with Sm-hPAF in a dose-dependent fashion. Platelet aggregation by the Sm-hPAF was totally inhibited by either PGE1, or GRGDS, but these reagents did not inhibit the platelet aggregation by collagen. 3) Histological examination of the rabbit skin sites showing an early reaction revealed increased dilatation of the veins and capillaries with cellular infiltration in the perivascular space of the dermis. Hyperplasia of the endothelial cells was noted. Degeneration of the vascular walls was observed in the later stages of the reaction. Aggregation of red cells in the vascular endothelium was also observed. Sm-hPAF was capable of producing vasculitis. 4) Twenty (76.9%) platelet-rich plasma samples (PRP) derived from 26 healthy human volunteers reacted with Sm-hPAF, but the remaining 6 PRPs were not reactive. Preliminary study suggests the existence of an inhibitory factor in plasma from nonreactive donors.
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PMID:[Purification and partial characterization of a novel human platelet aggregation factor in the extracellular products of Streptococcus mitis, strain Nm-65]. 898 63

We have previously demonstrated that arterial antigens derived from the aorta of spontaneously hypertensive rats (SHRs) stimulate arterial antigen-reactive T cell clones established from the spleens of SHR to proliferate and release cytokines. To identify immunogenic protein components associated with the arterial wall, arterial antigen-reactive T cell clones were tested against arterial antigens separated by SDS-PAGE and transferred to nitrocellulose. The greatest T cell reactivity was obtained with protein bands of molecular weight 66 kDa, 50 kDa, and 45 kDa. T cell clones reactive against the 50 and 45 kDa antigens from gels failed to respond to proteins of other molecular weight (M(r)) separated under reducing or nonreducing conditions, suggesting that these molecules are not subunits of larger proteins and may represent monomeric antigens polymerized into the arterial wall. These data suggest that certain epitopes of arterial wall antigens are immunogenic. T cells activated with these immunogenic epitopes could initiate or perpetuate vasculitis in the arteries of hypertensive rats.
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PMID:Characterization of arterial antigens using arterial antigen-reactive T cell clones from spontaneously hypertensive rats. 916 Jul 64

We report the case of a 32-year-old woman who had pruritic urticarial skin lesions associated with episodes of arthralgia. The first site affected by the eruption was the inside surface of the thighs; the patient also reported the presence of leukorrhea. The woman had previously been treated with H1 antagonist with moderate and transitory results; skin lesions reappeared just after the interruption of the treatment. Her biochemical data showed increased levels of erythrocyte sedimentation rate, blood eosinophilia and hypocomplementemia. Antinuclear antibodies, rheumatoid factor, cryoglobulins and serological diagnosis for hepatitis or mononucleosis viruses resulted negative. Considering the initial site of the cutaneous features and the presence of leukorrhea, we requested a vaginal smear and a culture of the cervical secretion, which revealed the presence of a Trichomonas infection. Furthermore, the SDS-PAGE revealed the presence of a molecular mass of 230,000 Da (230-kDa) in the serum, which indicated a Trichomonas surface protein. The following treatment with oral metronidazole caused the eradication of the Trichomonas infection after 3 weeks and subsequently the resolution of the urticarial clinical features. We wish to underline that in the presence of a case of urticaria vasculitis syndrome which seems to be without cause, it is important to investigate every diagnostic suspicion scrupulously.
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PMID:Urticaria from Trichomonas vaginalis infection. 1035 1

Local inflammatory reactions at the site of a mosquito bite are frequent. Immediate systemic reactions have occasionally been reported. The first case of a patient with relapsing episodes of a serum sickness-like syndrome following mosquito bites is reported herein. A 62-year-old patient came to the emergency room complaining of sudden malaise, chills, fever, headache, cervical lymph node enlargement, arthromyalgia, generalized purpura and leukopenia 6 h after a mosquito bite. He had experienced multiple similar episodes in the last 20 years, also following mosquito bites. Infectious and autoimmune diseases were ruled out. Serum IgE was 9,102 kU/l. Prick test of whole-body Culex pipiens extract was positive. Specific IgE to Aedes communis was 2.25 kU/l. SDS-PAGE immunoblotting of the patient's serum with whole-body C. pipiens extract revealed 43 and 17 kDa IgG-binding proteins and 22 and 17 kDa IgE-binding proteins, neither of which were found with control sera. Skin biopsy was consistent with leukocytoclastic vasculitis. The presence of both mosquito-specific IgE and IgG in the patient's serum suggest a possible cooperative immune response leading to clinical manifestations of serum sickness.
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PMID:Serum sickness-like syndrome due to mosquito bite. 1041 82

Anti-neutrophil cytoplasmic antibodies (ANCA) are a family of autoantibodies which react with components of phagocytic cells, and are associated with vasculitis and other idiopathic inflammatory disorders. However, the antigenic targets of many of these autoantibodies have not been defined yet. In this study, sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and isoelectric focusing (IEF) were evaluated for characterising the antigenic specificity of unidentified ANCA. The uncharacterised sera included those from patients with ulcerative colitis (n = 21), Crohn's disease (n = 5), cystic fibrosis (n = 16) and sarcoidosis (n = 2). In addition, sera from patients with antibodies to the phagocytic enzymes proteinase 3 (PR3) (n = 11) and myeloperoxidase (MPO) (n = 5) were also included. The sub-cellular localisation of antigens was determined by testing sera against crude neutrophil extract and sub-cellular fractions consisting of azurophilic granules, specific granules and cytosolic, fractions using enzyme-linked immunosorbent assays (ELISAs). All sera reacted with the crude and azurophilic granule extracts. The native system of IEF followed by capillary immunoblotting successfully detected anti-PR3 and anti-MPO in azurophilic granule extracts. In contrast, SDS-PAGE Western blotting failed to detect any reactivity, either to PR3 or MPO, in the crude extract or azurophilic granule extract. However, the antibody specificity of patient sera with uncharacterised autoantibodies could not be detected by IEF/capillary immunoblotting or SDS-PAGE. This study showed that the sub-cellular azurophilic granules are the antigenic target of a variety of uncharacterised ANCA. It also showed that IEF characterised both anti-PR3 and anti-MPO but failed to detect other forms of ANCA. In contrast, the majority of common ANCA were not detected by SDS-PAGE.
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PMID:Characterisation of anti-neutrophil cytoplasmic antibody target antigens using electrophoresis and western blotting techniques. 1043 39


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