Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0393754 (HSA)
 2,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty workers exposed to trimellitic anhydride (TMA) powder an phthalic anhydride (PA) fumes concurrently were evaluated by questionnaire and serum antibody studies. The study group was divided into high-an low-exposure groups on the basis of job descriptions and intensity of daily exposure. The questionnaire, which was designed to identify symptoms compatible with TMA-associated rhinitis, asthma, late respiratory systemic syndrome, and irritant responses, was administered to 18 of 20 workers. Total antibody binding was determined by the ammonium sulfate assay, and specific IgG and IgE binding was measured with an enzyme-linked immunosorbent assay (ELISA) to both PA-human serum albumin (PA-HSA) and TMA-human serum albumin (TM-HSA) conjugates. Specific IgE to TM-HSA was measured with the polystyrene-tube radioimmunoassay (PTRIA). The questionnaire identified nonirritant, immunologic symptoms caused by TMA primarily in the high-exposure group. Specific IgG, IgE, and total antibody binding to TM-HSA and PA-HSA were found exclusively in the high-exposure workers. One worker was identified with PA-associated rhinitis, high total antibody binding, and specific IgG and IgE to PA-HSA by means of the ELISA. The ELISA was as sensitive as the PTRIA in detecting the presence of specific IgE to TM-HSA. The present study demonstrates that an itemized questionnaire, combined with ELISA IgG and IgE determinations, may be a sensitive method for identifying workers who have or are at risk for developing TMA-induced respiratory symptoms.
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PMID:Clinical and immunologic evaluation of trimellitic anhydride-and phthalic anhydride-exposed workers using a questionnaire with comparative analysis of enzyme-linked immunosorbent and radioimmunoassay studies. 706 72

This article described our clinical and immunologic experience in assessing workers exposed to trimellitic anhydride (TMA) in three industrial settings. Since 1977 we have had engaged in a prospective study of workers involved at the site of manufacture of TMA. These studies demonstrate that serologic measurements of total antibody to trimellityl human serum albumin (TM-HSA) and IgE antibody to TM-HSA are predictive of the development of an immunologically mediated respiratory illness and are useful in monitoring workers removed from TMA exposure, in identifying asymptomatic workers who may be at risk in the future, and in defining the nature of sensitization of the work force. In a different industrial setting, we have been able to study workers who mixed previously manufactured TMA powder with epoxy resins. This study indicated that clinical assessments by a plant physician with a standardized questionnaire, along with serologic tests, could establish the presence or absence of an immunologic respiratory illness caused by the inhalation of TMA dust. In a third industrial situation, workers were exposed to both TMA and phthalic anhydride (PA). Here workers were interviewed by a local physician with minimal experience with TMA-related respiratory illness. In this situation a more detailed questionnaire was utilized, along with serologic tests utilizing the enzyme-linked immunosorbent assay to establish the presence of a TMA- or PA-related syndrome. Immunologic studies demonstrated in workers exposed to both TMA and PA that the antibody responses elicited showed little crossreactivity between antibodies directed against TM-HSA or PA-HSA.
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PMID:Clinical and immunologic evaluation of trimellitic anhydride workers in multiple industrial settings. 708 99

Native tetravalent Con A and the divalent acetylated derivative increased the hemolytic titer (i.e., the reciprocal of the antibody dilution required to give an average of one lytic site per sheep erythrocyte) of IgG antibodies against Forssman antigen by up to 225% with guinea pig and human complement. Although the average number of lytic sites generated at each antibody concentration increased, the slope of the titration curve did not change. Other lectins with the same or different sugar specificity either augmented or inhibited hemolysis but were less potent than Con A. Augmentation by Con A was consistent with the ability of lectin on the cell surface to bind but not activate guinea pig C1. Thus it appears that cell-bound Con A and IgG yield a complex that behaves like a doublet of IgG antibody molecules in its ability to fix and activate C1, when activation is dependent on the IgG component. In contrast, the highest dose of Con A inhibited by at least 50% the hemolytic activity of IgG antibodies against either a sugar-free protein (HSA) or a protein reactive with Con A (human myeloma IgE) using cells to which these antigens were coupled with chromic chloride. This suggests that the identity, density, and/or mode of presentation of the antigen on the cell surface may be important determinants of lectin-induced augmentation. Although both the enhancement or inhibition by Con A in the presence of whole C correlated with the number of C1 molecules bound and activated, there was no correlation with the ability of the lectin to agglutinate the cells.
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PMID:Enhancing effect of concanavalin A on the hemolytic activity of anti-Forssman IgG: the role of C1. 710 4

Twenty workers exposed to trimellitic anhydride (TMA) powder were evaluated to correlate respiratory symptoms with total antibody activity against trimellityl human serum albumin (TM-HSA). Further, specific IgG, IgA, and IgE against TM-HSA were compared to total specific antibody levels against that antigen. The workers were categorized clinically as having either the late respiratory systemic syndrome (LRSS), immediate rhinitis and asthma, or an irritant reaction. There were no histories compatible with the pulmonary disease--anemia syndrome. Total antibody and IgG antibody activity to TM-HSA correlated well (R8 = 0.75, p less than 0.05). Total antibody activity was found in almost all TMA-exposed workers, it did not discriminate the symptomatic workers from asymptomatic workers as well as did the IgG or total antibody determinations. IgE antibody activity against TM-HSA was elevated in one worker with immediate-type asthma. Previous studies correlated symptoms caused by TMA inhalation with antibody activity. This study indicates that clinical assessment plus total antibody determination or IgG antibody and IgE antibody determination should establish a means of diagnosis of the presence or absence of immunologic respiratory disease caused by TMA powder.
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PMID:Clinical and immunologic correlations in trimellitic anhydride airway syndromes. 726

The specificities of antibodies of different Ig classes against trimellityl (TM)-human serum albumin were examined by a radioimmunoassay inhibition technique. The antisera were from workers exposed to trimellitic anhydride who had 4 differing respiratory diseases. The studies demonstrated similarities between reactivities of antibodies of different Ig classes in these workers in that inhibition of antibody to TM-HSA required markedly less TM-HSA on a molar basis than TM-ovalbumin (OA) or sodium trimellitate (NaTM), the hapten for the trimellityl group. The results appears best explained by formation of new antigenic determinants on altered HSA molecules with the TM group forming a component of some of the new antigenic determinants. NaTM in high concentration could not completely inhibit the IgG antibodies of 2 sera suggesting either very low affinity for the hapten or that some of the antibodies might possibly be directed against new antigenic determinants formed from the reaction of TMA with HSA but that the TM group might not be a part of the antigenic specificity. The results of some studies also suggested that there were similar antigenic specificities on TM-HSA and TM-OA but of lesser concentration or lower affinity on the latter molecules. Passive transfer studies using a serum containing IgE antibodies against TM-HSA demonstrated that these human IgE antibodies will passively sensitize rhesus monkey skin. Neutralization of the cutaneous IgE antibodies occurred with TM-HSA but not with a great molar excess of NaTM in analogy with the in vitro studies.
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PMID:Human antibodies against trimellityl proteins: comparison of specificities of IgG, IgA and IgE classes. 729 21

Serum samples obtained from hemodialysis patients with immediate-type hypersensitivity reactions and hemodialysis patients with no reactions were analyzed for antibody activity against hapten-protein complexes prepared from PA and MDI. These chemicals, used in preparation of plastics, have been shown to be associated with immunologically mediated disease in other studies. IgE and IgG antibodies against P-HSA and MDI-HSA were detected in several sera, but symptomatic patients could not be differentiated from asymptomatic patients by antibody levels. Antibodies capable of agglutinating or hemolyzing P-E were also detected in some sera from hemodialysis patients. These studies demonstrate that although no clinical disease has yet been correlated with these antibodies, sufficient exposure of hemodialysis patients to protein-reactive chemicals occurs to elicit an immunologic response against hapten-protein or hapten-cells. Such antibodies may have immunopathogenetic significance in subjects systemically exposed to fluids which have been in contact with plastics.
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PMID:Antibodies in hemodialysis patients against hapten-protein and hapten-erythrocytes. 740 Jun 67

Immunization of mice for contact sensitivity induces two different antigen-specific Thy-1+ cell activities that are required to act in sequence for elicitation of contact sensitivity. In this study, 2,4-dinitro-1-fluorobenzene contact sensitivity responses in BALB/c and C3H/He mice demonstrated the importance of early-acting and antigen-specific contact sensitivity-initiating cells to recruit the classical, late-acting contact sensitivity effector T cells. Employing in vitro treatment of sensitized cells with monoclonal antibodies to cell surface determinants and then incubation in complement, prior to adoptive cell transfer, the contact sensitivity-initiating cells were shown to have a surface phenotype that is quite unusual for antigen-specific cells [Thy-1+, CD5+, CD3-, CD4-, CD8-, sIg-, B220+, major histocompatibility complex class II-, CD23+, IL-2R-, IL-3R+, Mel-14-, CD44+ (Pgp-1+), J11d+ (HSA+), MAC-1+, LFA-1+, and Fc gamma IIR+], and is quite different from the late-acting, contact sensitivity-effector T cells (Thy-1+, CD5+, CD3+, CD4+, CD8-, sIg-, B220-, major histocompatibility complex class II-, CD23-, IL-2R+, IL-3R-, and CD44- (Pgp-1-), J11d-(HSA-), MAC-1-, LFA-1+, Fc gamma IIR-). Contact sensitivity initiation was required for elicitation of late 24-h 2,4-dinitro-1-fluorobenzene contact sensitivity responses, in both BALB/c and C3H/He mice. Moreover, relatively high doses of some monoclonal antibodies [anti-B220 (CD45RA) and anti-CD23 (IgE Fc epsilon II receptor)] were necessary to completely eliminate all contact sensitivity-initiating cells that permitted expression of late contact sensitivity-effector T-cell activity. In contrast, high doses of monoclonal antibody specific for surface determinants of late-acting contact sensitivity effector T cells (anti-CD3 and anti-CD4), when used in high doses similar to anti-B220 and anti-CD23, had no effect on contact sensitivity-initiating cell activity. Our results indicate that two very different antigen-specific Thy-1+ cells are necessary to elicit 2,4-dinitro-1-fluorobenzene contact sensitivity in BALB/c and C3H/He mice.
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PMID:DNFB contact sensitivity (CS) in BALB/c and C3H/He mice: requirement for early-occurring, early-acting, antigen-specific, CS-initiating cells with an unusual phenotype (Thy-1+, CD5+, CD3-, CD4-, CD8-, sIg-, B220+, MHC class II-, CD23+, IL-2R-, IL-3R+, Mel-14-, Pgp-1+, J11d+, MAC-1+, LFA-1+, and Fc gamma RII+). 750 36

On the basis of the selection of a population of patients intolerant to sulfites by the clinical history, a simple blind oral provocation test and a basophil activation test, we explored the basophil activation reaction induced by sulfites after passive sensitisation of blood donors basophils. We demonstrated that the percentages of activation obtained with a non covalent reagent (MBS-HSA), a covalent reagent (sulfonyl-HSA) and the optimal concentration of an anti-IgE were not significantly different. Human basophil activation was negativated by heating the transferred sera and by competition with a monoclonal human IgE. We also observed mediator release (histamine and LTC4) with a low frequency, histamine release being strictly related to the carrier protein concentration. In two cases, sulfite specific IgE were detected by ELISA. These results are in favour of the specificity and the IgE dependent nature of basophil activation induced by sulfites.
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PMID:[Demonstration of sulfite-group-specific IgE in patients with intolerance to preservatives]. 751 36

Diisocyanate-induced asthma differs from occupational asthma (OA) caused by protein allergens in that specific IgE antibody responses are rarely identified. To investigate the immunopathogenesis of diisocyanate asthma, diisocyanate-exposed workers were evaluated for in vitro production of antigen-specific mononuclear cell-derived histamine releasing factor (HRF). The mean HRF response to diisocyanate-HSA antigens was significantly greater in patients with OA than in diisocyanate-exposed asymptomatic subjects (p < 0.05). No association was found between HRF and diisocyanate-specific antibodies. Analysis of HRF production by subpopulations of peripheral blood mononuclear cells (PBMC) showed that lymphocytes and adherent cells were major sources of both spontaneous and antigen-stimulated HRF. The results suggest that antigen-specific HRF produced by PBMCs are an important biomarker for diisocyanate-induced asthma. This is the first report of hapten-specific stimulation of PBMCs resulting in HRF production.
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PMID:Antigen-specific stimulation of histamine releasing factors in diisocyanate-induced occupational asthma. 752 54

On the basis of the CD 63 bi-modal expression on the membrane of activated basophils, we set up a flow cytometric method for the analysis of human basophils activation by an anti-IgE and anti-CD 63 double labelling. We demonstrated that the statistical characteristics of the percentages of activation obtained by an anti-IgE stimulation allowed the use of this method for pharmacological studies. The percentages of activation were of the same order of magnitude than those obtained by histamine release. CD 63 expression was also observed for a low affinity allergen such as the sulfonyl-HSA conjugate used for sulfites hypersensibility diagnosis, healthy donors being negative. This method, which can be automatized may represent an interesting candidate in the field of hapten hypersensitivity which lacks of reliable diagnostical methods.
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PMID:[Analysis of membrane expression of the CD63 human basophil activation marker. Applications to allergologic diagnosis]. 752 23


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