Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Goodpasture's syndrome has characteristically been described as being mediated by IgG antibodies. We have recently seen a 55-year-old man who developed renal failure and hemoptysis; a renal biopsy showed linear deposits of IgA and C3 involving glomerular and tubular basement membrane. Serologic tests for detecting (IgG) antiglomerular basement membrane antibodies were negative. Elution studies of kidney and lung showed the presence of an IgA antibasement membrane antibody only. The patient's serum contained IgA, but not IgG, antibodies reactive with glomerular and tubular basement membrane of normal human kidney and alveolar basement membrane of normal human lung. Attempts to transfer disease with the patient's IgA antibody to a monkey and to Lewis and Brown-Norway rats were unsuccessful. Immunoglobulin A antibasement membrane antibody must be considered in the design of immunoserologic procedures for the diagnosis of Goodpasture's syndrome.
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PMID:IgA antibasement membrane nephritis with pulmonary hemorrhage. 11 92

Secretory IgA is the dominant immunoglobulin produced in the small intestine and one important component of the local defense against dietary and infectious agents present in the gut lumen. The effect of small intestine transplantation on total production of sIgA and on the response to a newly presented antigen, cholera toxin, was determined in a rat segmental heterotopic intestinal transplant model. Lewis x Brown Norway F1 (LBNF1) allografts in Lewis hosts made normal amounts of sIgA, when compared with LBNF1 Thiry-Vella loops or LBNF1 isografts. In contrast, the allografts failed to make a significant specific sIgA response when immunized with cholera toxin at days 0 and 7 following transplantation. This failure was not the result of surgical manipulation, as isografts made normal amounts of specific sIgA directed against cholera toxin. Cyclosporine immunosuppression delayed, but did not prevent, the secretion of specific antibody in isografts. This failure to respond to a new antigen may have important implications for the safety of small bowel transplantation.
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PMID:Immune function in transplanted small intestine. Total secretory IgA production and response against cholera toxin. 230 56

Protein-loss into the gastrointestinal tract is a feature of many different diseases, a number of which are immunologically mediated, e.g. systemic lupus erythematosus or Crohn's disease. The pathogenic mechanism of protein-losing enteropathy in diseases without obvious enterocyte injury are unknown. Brown-Norway-rats (BN-rats) were gavaged with low doses of HgCl2 for 39 weeks. Within 2 weeks, the intestines showed strong linear staining for IgG and IgA along vascular and intestinal basement membranes. Granular deposits containing IgG and C3 were present along intestinal basement membrane only in the late stages of the experiment; only in these animals increased intestinal protein loss as measured by fecal Cr-51 excretion was found. These findings suggest that immune complex deposition along the intestinal basement membrane can lead to protein-losing enteropathy. This disease may be used as a model for the study of immunologically mediated intestinal disease.
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PMID:[Mercuric chloride-induced enteropathy in the rat: a model of gastrointestinal disease with immunologic pathogenesis]. 296 59

Only few reports are available on the consequences of chronic oral administration of low doses of mercuric chloride (HgCl2). Forty Brown-Norway rats received 150 micrograms HgCl2/100 g body weight 3 times a week by gavage or by i.m. injection with 100 micrograms twice per week. After 2 weeks of oral HgCl2 administration, the rats lost weight and hair. Phases of proteinuria were observed in weeks 5-8 and then continuously from week 12 until the end of the experiment at week 39. Antibodies binding to renal, intestinal, and vascular basement membrane developed after 2 weeks; circulating immune complexes were detectable in increasing titers starting at week 3. There were linear deposits of IgG, IgM, and IgA in the glomerular basement membrane and tubular basement membrane, and along the intestinal basement membrane. After week 11, the first granular immune deposits were observed in renal and intestinal basement membranes. Light microscopy showed thickening of glomerular basement membrane, mesangial matrix, and tubular basement membrane. In addition, interstitial nephritis was observed in some animals. Interestingly, kidney involvement was as severe in the orally as the i.m.-treated animals.
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PMID:Autoimmune disease induced by oral administration of mercuric chloride in Brown-Norway rats. 353 91

In Brown-Norway (BN) rats, oral administration of mercuric chloride (HgCl2) induced morphological lesions of the ileum and, in lesser degree, of the colon, with abnormal deposits of IgA in the basement membranes of intestinal glands and of IgG in the basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and with the lamina propria of a normal BN rat was found in the serum and IgG deposits were present in renal glomeruli of BN rats receiving HgCl2. Thus, it is conceivable that the deposits of IgG present in the intestine resulted from local fixation of circulating autoantibodies. In contrast, IgA with basement membrane reactivity was not detected in the sera nor in the renal glomeruli, suggesting that the intestinal deposits of IgA were formed in situ. This IgA-IgG intestinal disease inducible in BN rats may provide a model for the study of alterations of the secretory IgA system, as well as for testing the possibility that abnormal deposits IgA-IgG in the intestinal structures are associated with local functional changes.
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PMID:IgA-IgG disease in the intestine of Brown-Norway rats ingesting mercuric chloride. 623 Jan 86

Immune hypersensitivity to house dust mite antigen (HDM) is a frequent cause of respiratory allergy. The objective of this study was to determine whether exposure to NO2, a common indoor air pollutant, modulates immune responses to HDM and influences immune-mediated lung disease. Brown Norway rats were immunized ip with 100 micrograms semipurified antigen and Bordetella pertussis adjuvant and challenged 2 weeks later with an intratracheal injection of 50 micrograms of a crude antigen preparation. Exposure to 5 ppm NO2 for 3 hr after both immunization and challenge procedures resulted in significantly higher levels of antigen-specific serum IgE, local IgA, IgG, and IgE antibody than air controls, and increased numbers of inflammatory cells in the lungs. Lymphocyte responsiveness to antigen in the spleen and MLN was also significantly higher in NO2-exposed animals. These data show that exposure to a common air pollutant can upregulate specific immune responses and subsequent immune-mediated pulmonary inflammation.
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PMID:Increased immune and inflammatory responses to dust mite antigen in rats exposed to 5 ppm NO2. 899 54

The determination of an appropriate period of duration for specific immunotherapy presents an important problem in the treatment of allergic diseases. The aim of this paper was to conduct a prognostic study of certain immunological indicators after 4 years of desensitization, and to determine which of the tested indicators are characteristic for an evaluation of the clinical condition. Individuals with pollinosis were tested after the first, second, third and fourth year of desensitization using the pollen allergen. The B and T-lymphocyte counts, the levels of immunoglobulins A, M, G, and total and specific E, and the volume of basal, total and specifically released histamine were all measured. Furthermore, the clinical condition of the patient was defined using a score method (0-3 points), taking into account the results of testing and the basic symptoms of the disease. Following this, a prediction of results after the fifth year of desensitization was made, using Brown's method of exponential smoothing. The majority of the data obtained from the forecasting study indicate that in the subsequent fifth year of desensitization, the indicators studied should undergo further changes in values, offering a strong argument for the necessity of extending the period of immunotherapy in pollinosis beyond three years. In the results of the regression function estimates it was determined that, among the indicators studied, those which are helpful in monitoring treatment are: T-RFC, T-FcG-BG, T-FcM-EN and B-EAC lymphocyte counts, levels of IgA, IgM and specific IgE, and the percentage of specifically released histamine.
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PMID:Specific immunotherapy in pollinosis: II. Forecasting changes in certain cytoimmunological indicators after four years of immunotherapy in pollinosis. 901 80

A molecularly cloned attenuated strain of Venezuelan equine encephalitis virus (VEE) has been genetically configured as a replication-competent vaccine vector for the expression of heterologous viral proteins (N. L. Davis, K. W. Brown, and R. E. Johnston, J. Virol. 70:3781-3787, 1996). The matrix/capsid (MA/CA) coding domain of human immunodeficiency virus type 1 (HIV-1) was cloned into the VEE vector to determine the ability of a VEE vector to stimulate an anti-HIV immune response in mice. The VEE-MA/CA vector replicated rapidly in the cytoplasm of baby hamster kidney (BHK) cells and expressed large quantities of antigenically identifiable MA/CA protein. When injected subcutaneously into BALB/c mice, the vector invaded and replicated in the draining lymphoid tissues, expressing HIV-1 MA/CA at a site of potent immune activity. Anti-MA/CA immunoglobulin G (IgG) and IgA antibodies were present in serum of all immunized mice, and titers increased after a second booster inoculation. IgA antibodies specific for MA/CA were detected in vaginal washes of mice that received two subcutaneous immunizations. Cytotoxic T-lymphocyte responses specific for MA/CA were detected following immunization with the MA/CA-expressing VEE vector. These findings demonstrate the ability of a VEE-based vaccine vector system to stimulate a comprehensive humoral and cellular immune response. The multifaceted nature of this response makes VEE an attractive vaccine for immunization against virus infections such as HIV-1, for which the correlates of protective immunity remain unclear, but may include multiple components of the immune system.
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PMID:Humoral, mucosal, and cellular immunity in response to a human immunodeficiency virus type 1 immunogen expressed by a Venezuelan equine encephalitis virus vaccine vector. 906 Jun 63

It has been suggested that airway irritation, by acting as an adjuvant, as well as producing damage, may be an important factor related to asthma. The present study examined the window of time following acute upper and lower airway irritant exposure to determine the period of increased risk of immunological sensitization. Brown Norway rats were exposed to 87 ppm NO2 or 1000 ppm NH3 for 1 hr. A 30-min ovalbumin (OVA) exposure of 18.14 microg/liter air was given at various times based upon the time course of irritant associated inflammatory response (either immediately prior to or 1 or 7 days after the irritant exposure). OVA-only, NO2-only or NH3-only controls, and saline controls were also studied. Weekly booster exposures of OVA (or saline) were given. Circulating OVA-specific IgE, IgA, and IgG levels were quantified periodically during the 6 weeks of the study. Bronchoalveolar lavage (BAL) was also performed to examine the inflammatory response to allergic and irritant challenge. Significant increases in OVA-specific IgE, IgG, and IgA antibody titers were seen in rats given the sensitizing OVA exposure within 1 day of the NO2, but not NH3 exposures. Enhancement of cellular infiltrate in BAL was noted in groups given the sensitizing OVA exposure within 1 day of the NO2 or NH3. It is concluded that the inflammatory and immunological response to antigen exposure can be modified by the site of respiratory tract irritation and the relative times of irritant and antigen exposure.
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PMID:Adjuvant effect of respiratory irritation on pulmonary allergic sensitization: time and site dependency. 919 20

The complete genomic sequence of a bovine C alpha gene is reported here. The genomic sequence was obtained from a C alpha phage clone that had been cloned from a genomic EMBL4 phage vector library. The C alpha sequence had previously been expressed as a chimeric antibody and identified as IgA using IgA-specific antibodies. Intron/exon boundaries were determined by comparison of the genomic sequence with an expressed bovine C alpha sequence obtained from spleen by reverse transcription-polymerase chain reaction (RT-PCR). Analysis of 50 Swedish bovine genomic DNA samples using genomic blots and five different restriction enzymes failed to detect evidence of polymorphism. However, PstI digests of Brown Swiss DNA showed a restriction fragment length polymorphism (RFLP), suggesting that at least two allelic variants of bovine IgA exist. Comparison of the deduced amino acid sequence of bovine IgA with sequences available for other species indicated that the highest homology was with that of swine, another artiodactyl. This was the highest homology observed for all mammalian IgA compared except for that between IgA1 and IgA2 in humans. Bovine IgA shares with rabbit IgA3 and IgA4, an additional N-linked glycosylation site at position 282. However, the collective data indicate that cattle are like swine and rodents and unlike rabbits in having a single locus of the gene encoding IgA of this species.
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PMID:Characterization of the bovine C alpha gene. 920 58


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