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)

A case of an anaphylactic shock following topical application of chlorhexidine preparation is reported. Specific skin-sensitizing antibodies against chlorhexidine were demonstrated in the serum from the patient by a passive transfer test. IgE antibodies against chlorhexidine were also detected by radioallergosorbent technique (RAST). Paper discs conjugated with chlorhexidine-HSA (human serum albumin) significantly bound the IgE antibodies. Furthermore, all of the sera from seven other patients with shock reactions following the topical application of chlorhexidine preparation also showed high RAST counts. Both chlorhexidine gluconate and chlorguanide which represents approximately half a molecule of chlorhexidine inhibited the reaction in a dose-dependent fashion. It is suggested that the shock reactions following topical application of chlorhexidine are mediated by IgE antibodies against chlorhexidine and that chlorhexidine and chlorguanide share the same antigenic determinant.
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PMID:IgE antibody-mediated shock reaction caused by topical application of chlorhexidine. 242 71

A rhesus monkey model was developed to demonstrate the pathogenetic role of IgE to chemical hapten-protein conjugates in causing human occupational asthma from reactive chemicals. Serum from a worker with trimellitic anhydride (TMA) asthma that contained high titers of IgE, IgG, IgM, and IgA to trimellityl-human serum albumin (TM-HSA) was aerosolized into the lungs of two monkeys to afford passive airway sensitization. After the monkeys were challenged with aerosolized TM-HSA, pulmonary functions demonstrated acute airway responses similar to that of Ascaris antigen-induced, IgE-mediated bronchospasm in Ascaris-sensitive monkeys. The monkeys had no airway reactivity when challenged with TM-HSA 1 week after the first positive TM-HSA response elicited with passive sensitization. Passive cutaneous reactivity to TM-HSA was also elicited by the donor serum, but heat-treated donor serum failed to confer cutaneous or bronchial reactivity. These results indicate that airway reactivity in this passive-transfer monkey model of TMA asthma is an antigen-specific response mediated by heat-labile serum factors, presumably IgE to TM-HSA, and does not occur by irritant mechanisms. This experimental model could become a valuable system for evaluating the role of IgE to hapten-protein conjugates in the immunopathogenesis of asthma caused by other reactive chemicals capable of acting as haptens. We postulate that immunologic and clinical features should be consistent with asthma caused by such reactive chemicals and mediated by such mechanisms.
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PMID:Induction of antigen-specific bronchial reactivity to trimellityl-human serum albumin by passive transfer of serum from humans to rhesus monkeys. 245 Sep 39

Desensitization of human basophils with anti-IgE antibody or antigen induced an increased sensitivity to the phorbol ester TPA, evidenced as 2-5 fold increase in the potency of TPA to induce histamine release. As noted in previous publications the magnitude of the change in sensitivity to TPA was a function of the extent of cell surface IgE crosslinking. Thus, the density of cell surface antigen-specific IgE determined the magnitude of the curve shift and the multivalent antigen, BPO21-HSA was found to produce a greater curve shift than the simpler bivalent hapten, BPO2, in accord with previous studies which demonstrated that BPO2 was a "weak" stimulus compared to BPO21-HSA. Basophils which had been fully desensitized by prior treatment with anti-IgE or antigen in the absence of calcium also displayed the curve shift for at least 24 h after desensitization. However, the change induced by crosslinking which altered the cells' sensitivity to TPA required the continued presence of crosslinks and was therefore not the result of a permanent alteration induced by desensitization. Basophils which were fully desensitized to BPO7-HSA demonstrated the curve shift provided that the antigen-induced crosslinks were maintained: treatment with monovalent hapten, BPO-EACA, rapidly returned the cell response to TPA to control, non-desensitized, levels. Since TPA is thought to act by activation of protein kinase C (PKC) we demonstrated that BPO-HSA induced crosslinking increased PKC activity and that the increased activity persisted unless antigen-induced crosslinks were dissociated by the addition of monovalent hapten.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistence of early crosslink-dependent signal transduction events in human basophils after desensitization. 245 86

Using a self-made bag inhalation challenge device. We diagnosed 12 TDI asthmatics, who were from 18 symptomatic workers. Of the 12 cases there were three types of airway reaction to TDI: three showed an immediate response; six, a late response; three, a dual response. After inhalation challenge, FEV1 PEFR, V50, and V25 descended obviously, suggesting that airway response to TDI in TDI asthmatics might occur in either larger or small airway. As a result of methacholine challenge nonspecific bronchial reactivity in 12 TDI asthmatics was markedly increased. After inhalation of TDI, the further descending of PC20 FEV1 showed that TDI could increase airway reaction to methacholine. Patients received skin test with TDI-HSA conjugate. There were positive response in 11 of the 12 TDI asthmatics and in 11 of the 62 TDI workers who had no symptoms after exposure to TDI, and no positive response in 18 common asthma patients. Therefore, TDI-HSA skin test can be used to a assist diagnosis of TDI asthma and a differential diagnosis from ordinary asthma. Specific IgE antibody levels showed no difference between TDI asthma and normal control group before TDI challenge. A marked increase in TDI asthma occurred after TDI challenge.
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PMID:[Occupational toluene diisocyanate (TDI) asthma--inhalation challenge test and TDI-HSA (human serum albumin) skin test and detection of specific IgE]. 255 81

Biochemical mechanisms of desensitization were explored by using peritoneal mouse mast cells saturated with monoclonal mouse IgE anti-DNP antibody. It was found that a 1-min incubation of the sensitized cells with 0.01 micrograms/ml DNP-HSA in the absence of Ca2+ was sufficient to desensitize the cells completely. The treated cells failed to release a detectable amount of histamine upon incubation with an optimal concentration (0.1 to 1.0 micrograms/ml) of DNP-HSA and Ca2+. Determination of the number of antigen molecules bound to mast cells revealed that only a small (less than 10%) fraction of cell-bound IgE antibody molecules reacted with desensitizing antigen, and that desensitized cells and untreated (sensitized) cells could bind comparable amounts of antigen upon incubation with rechallenging antigen. However, the binding of antigen molecules to desensitized cells failed to induce any of the early biochemical events, i.e., phospholipid methylation, cAMP rise, and 45Ca uptake, as well as histamine release. It was also found that intracellular cAMP levels in desensitized cells were comparable to those in sensitized cells. Desensitization by a suboptimal concentration of DNP-HSA was prevented by inhibitors of methyltransferases, such as 3-deaza adenosine plus L-homocysteine thiolactone. Sensitized cells pretreated with 0.01 micrograms/ml DNP-HSA in the absence of Ca2+ and in the presence of the methyltransferase inhibitors responded to an optimal concentration of antigen for histamine release when they were rechallenged in the presence of Ca2+. Inhibition of desensitization by methyltransferase inhibitors was reversed by the addition of S-adenosyl-L-methionine to the system. The results indicated that the activation of methyltransferases, induced by receptor bridging, is involved in the process of desensitization. Desensitization was inhibited by reversible inhibitors of serine proteases, such as p-aminobenzamidine, indole, and synthesized substrates of rat mast cell proteases. It was also found that diisopropylfluorophosphate (DFP), an irreversible inhibitor of serine proteases, completely blocked desensitization at the concentration of 10 to 40 nM. This concentration of DFP did not affect the antigen-induced histamine release, whereas 100- to 1000-fold higher concentrations of DFP did inhibit histamine release. The results suggest that serine proteases are involved in both the induction of histamine release and desensitization, and that the protease involved in desensitization is distinct from that involved in triggering histamine release.
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PMID:Biochemical analysis of desensitization of mouse mast cells. 258 46

IgE antibodies to the antiseptic agent chlorhexidine have recently been detected in the majority of sera from a small group of predominantly Japanese individuals showing anaphylactic-type adverse reactions towards chlorhexidine. In this study the prevalence of IgE and IgG antibodies with specificity for chlorhexidine was investigated in groups of Japanese and British individuals. The RAST data, using a better defined semi-chlorhexidine-HSA antigen than previously employed, revealed that chlorhexidine-specific IgE was only detected in Japanese individuals who had experienced anaphylactic-type reactions and was not detected in groups of Japanese nurses and patients, or in groups of British nurses and hospital staff, all in regular contact with chlorhexidine. A group of British blood donors was also negative. In contrast, IgG antibodies were detected not only in sera from chlorhexidine-sensitive Japanese patients, but also in several sera from Japanese nurses, non-sensitive Japanese patients and several British individuals. The possible reasons for these observations are discussed.
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PMID:The incidence of IgE and IgG antibodies to chlorhexidine. 266 Sep 69

All 306 South African platinum refinery workers (116 white, 190 coloured) accepted for employment on grounds of absence of evidence of atopy were investigated using the skin prick test and RAST to detect sensitivity to platinum, palladium, and rhodium salts. RAST studies were made for these, together with HSA and DNP-HSA RAST. Of the 306 workers, 38 had a positive skin prick test to the platinum halide salts; of these, one gave a positive reaction to the palladium salt and six to the rhodium salt. There were no isolated positives to the rhodium and palladium halide salts. Total IgE levels were raised in 24 of the 38 (63%) platinum salt prick test positive workers compared with only 43 of the 268 (16%) prick test negative group (p less than 0.001). Positive RASTs were obtained in 62% of those with positive skin tests to the platinum salts. Four of the six giving positive rhodium salt skin tests gave a positive RAST to rhodium salt. Of these, two gave positive RASTS to HSA and all four to DNP-HSA. The palladium salt RAST was negative in the single skin test reactor. In the platinum salt skin test positive group a raised HSA RAST was obtained in 10.5% compared with only 2.5% in the skin negative group. Twenty one per cent of the platinum salt skin positive group had a raised RAST score to DNP-HSA with only 3.5% (4/116) in the skin test negative group, of whom three also had a raised HSA RAST. The latter findings are suggestive of IgE antibody production to new antigenic determinants in HSA produced by conjugation with the platinum salts.
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PMID:IgE antibody responses to platinum group metals: a large scale refinery survey. 293 74

Six patients with multiple subjective health complaints, which have been correlated with chronic exposure to formaldehyde during the course of their education and occupations, were tested for the existence of antibodies (IgE, IgM, and IgG) to formaldehyde (F) conjugated to human serum albumin (F-HSA). In addition, the percentage and absolute numbers of peripheral lymphocyte subpopulations as determined by surface markers were investigated. Antibody titers to F-HSA were present as follows: IgE (2 patients), IgM (3 of 4 tested patients), and IgG (5 patients). Analysis of lymphocyte subpopulations showed T-helper/suppressor (H/S) ratios ranging from 0.8 to 3.3. All 6 patients had elevated Tal cells (antigen memory cells), whereas interleuken 2 receptor positive cells were within expected values. Following formaldehyde exposure, 5 of the patients complained of an initial flulike illness from which they have not completely recovered. The sixth individual had a history of recurrent respiratory infections and surgical removal of hyperplastic ethmoid sinus tissue. The common occurrence of anti-F-HSA antibodies, flulike illness, and Tal cells are interpreted as suggestive of a chronic antigenic stimulation of the immune system in these 6 patients. Further immunological work-up of additional subjects and immune parameters with similar history of formaldehyde exposure and subjective health complaints is warranted.
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PMID:Antibodies and immune profiles of individuals occupationally exposed to formaldehyde: six case reports. 297 32

Evaluation of the immunologic contribution to the pathogenesis of isocyanate lung disease necessitates preparation of isocyanate-protein conjugates to detect anti-isocyanate antibodies. The preparation and characterization of the conjugates were described in the preceding paper in this issue. Sera were obtained from two guinea pigs immunized with 4,4'-diisocyanatodiphenylmethane (MDI) and from three workers with occupational exposure to MDI. By use of Western blot analysis, guinea pig IgG antibodies were best detected by the monomeric component of MDI-guinea pig serum albumin. ELISA additionally indicated that conjugates which contained a high density of hapten detected greater amounts of antibody than did conjugates containing low amounts of hapten. The same procedures were then used to assess the amount of MDI-specific IgG and IgE antibody in sera from symptomatic workers. Effective MDI-HSA antigens were those that were monomeric and had high haptenic content. Highly substituted conjugates of monoisocyanates (phenyl isocyanate and p-tolyl isocyanate) with serum albumins were also effective in detecting antibodies to MDI. These results indicate the importance of the composition of isocyanate conjugate antigens in detecting antibodies to diisocyanates and suggest that standards be developed for preparation and characterization of these diagnostic serologic reagents.
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PMID:Diisocyanate antigens that detect specific antibodies in exposed workers and guinea pigs. 297 45

A case of allergic oculorhinitis induced by toluene diisocyanate (TDI) exposure in a subject who two years later developed bronchial asthma due to TDI is described. A 55-year-old nonatopic spray painter developed symptoms of oculorhinitis two or three hours after direct occupational exposure to polyurethane varnish; at the first examination neither specific nor nonspecific bronchial hyperresponsiveness was present. Two years later the patient, who had remained in his job, developed episodic dyspnea, wheezing, and cough immediately after TDI exposure, with persistence of oculorhinitis; at this time a slight immediate-type response to a specific bronchial provocative test with polyurethane varnish and TDI was observed. Nonspecific bronchial hyperresponsiveness was mild. Specific IgE to TDI-HSA conjugate was present at both the first and second examinations. We conclude that, in some cases, TDI may cause "allergic" oculorhinitis and bronchial asthma, probably with an immunological IgE-mediated mechanism.
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PMID:TDI-induced oculorhinitis and bronchial asthma. 298 3


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