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Biomedical subjects

J J Pruzansky

Publications and source records attributed to J J Pruzansky.

At least 55 records · Page 3Linked to original sources
PubMed1978

Human antihapten antibodies in trimellitic anhydride inhalation reactions. Immunoglobulin classes of anti-trimellitic anhydride antibodies and hapten inhibition studies.

Inhalational exposure to trimellitic anhydride (TMA) produces an immediate-type asthmatic or a late respiratory systemic syndrome in certain workers after a latent period of work exposure. TMA has been found to react with proteins to produce a hapten-protein complex (trimellitate [TM] protein) or become hydrolyzed in aqueous, alkaline solutions to produce a salt, NaTM. Using a solid-phase radioimmunoassay technique, antibodies of different Ig classes were detected against TM-protein conjugates. IgE antibody was detected in three of five workers with asthma. IgG and IgA antibodies were detected in most exposed workers but higher levels of antibody were found in symptomatic workers even after long periods without direct TMA exposure. IgM antibody activity against TM-human serum albumin (TM-HSA) was detected but did not differentiate symptomatic from asymptomatic workers. NaTM served as a hapten for study because it does not react with proteins to form a hapten-protein complex as TMA does. The NaTM only partially inhibited IgG antibody activity against TM-HSA and much smaller amounts of TM-HSA than of NaTM were required to neutralize IgG antibody. A similar result was found with TM-ovalbumin. The latter results suggest that some IgG antibody is directed against a TM-protein moiety, probably a TM-amino acid determinant. In contrast to IgG, marked inhibition by NaTM of IgA and IgM antibody against TM-HSA was found in the sera studied.

Anhydrides↗
PubMed1977

Trimellitic anhydride-induced airway syndromes: clinical and immunologic studies.

This report describes a spectrum of respiratory symptoms in workers exposed to trimellitic anhydride (TMA), a biologically reactive chemical used in the plastics industry. Fourteen workers who had worked on a unit which synthesized TMA were evaluated by clinical and immunologic methods. Respiratory syndromes induced by TMA inhalation included asthma and rhinitis of the immediate type, late onset asthma with systemic symptoms, and airway irritation. TMA was shown to couple rapidly to human serum albumin, forming an immunoreactive hapten-protein complex. The workers' immunologic reactivity to this complex could be quantitated and correlated with the three respiratory syndromes. The asthma-rhinitis syndrome was mediated by IgE antibody specific for the TMA hapten. The syndrome of late onset asthma with systemic symptomes was accompanied by elevated levels of TMA-specific IgG antibody. Rheumatoid factor in high titer was found in one worker with IgE-mediated asthma and in two workers with asthma of late onset. Lymphocyte reactivity of TMA-HSA was demonstrated in three workers representative of the three clinical syndromes. Leukocyte histamine release was demonstrated to TMA-HSA in one worker with high levels of IgE antibody specific for TMA-HSA who had severe symptoms of acute rhinitis and asthma.

Adult↗
PubMed1977

Polymerization of mixtures of grass allergens.

Mixed grass pollen allergens were precipitated from crude grass extract by 90% saturation with ammonium sulfate. The precipitate was dissolved and polymerized with glutaraldehyde. Polymerized allergens with a molecular weight range of 200,000 to 4,000,000 were isolated. The resultant grass allergen polymers had reduced allergenicity but were capable of absorbing out IgG antibody from sera of 2 patients treated with crude grass allergens. This alteration of allergenicity was intended to reduce the ability of allergens to react with IgE-sensitized cells rather than to modify or destroy antigenic determinants. Prior exposure of allergens to phenol used as a preservative inhibited the polymerization process probably by blocking combining sites with which glutaraldehyde reacts.

Allergens↗
PubMed1977

Studies of perennial ragweed immunotherapy.

Perennial ragweed immunotherapy was studied in 24 patients with ragweed pollenosis. Cellular responsiveness was determined by measuring the cellular reactivity and sensitivity to ragweed antigen E (RW-AgE) by RW-AgE-induced leukocyte histamine release. Serum blocking antibody content was determined by measuring the serum RW-AgE binding capacity by ammonium sulfate coprecipitation of bound RW-AgE. Specific IgE (anti-RW-AgE) concentration was determined by polystyrene tube radioimmunoassay. Cellular responsiveness decreased with continuing immunotherapy, as did the specific IgE concentrations. The serum RW-AgE binding capacity, in contrast, increased as treatment continued. The absence of demonstrable correlations between RW-AgE binding capacity and cellular reactivity, cellular sensitivity, and specific IgE concentrations contrasted impressively with the demonstration of multiple significant correlations between the change in the RW-AgE binding capacity and the other parameters studied. The degree of increase in RW-AgE binding capacity correlated significantly with the degree of decrease in both the specific IgE concentration (p is less than 0.04) and the cellular sensitivity to RW-AgE (p is less than 0.003). these findings suggest that the active process of blocking antibody production, rather than the passive presence of blocking antibody, is related to the process which decreases the specific IgE concentration and the degree of cellular responsiveness and therefore results in clinical improvement.

Adolescent↗
PubMed1977

Living histamine-containing cells from the bronchial lumens of humans. Description and comparison of histamine content with cells of rhesus monkeys.

Cell populations obtained by bronchial lavage from human subjects were examined for the presence of cells related to the mast cell-basophil series. Such bronchial lumen histamine-containing cells (BLHCC) were identified. The BLHCC stained with toluidine blue may be identified by bright field or dark field microscopy. The BLHCC are alive as evidenced by ability to release histamine (H) after exposure to anti-IgE or calcium ionophore. Although H release from peripheral blood leukocytes by these two agents is potentiated by the presence of D2O, H release from BLHCC of the same subjects by anti-IgE or calcium ionophore was not potentiated by D2O. In studies comparing bronchial cell populations of humans and rhesus monkeys with peripheral blood leukocyte populations of the same subjects, the histamine content of the bronchial cell population was much higher in rhesus monkeys. IgE/Alb ratios of respiratory secretions and serum of the same human subjects were of the same order of magnitude in contrast to previous comparisons done on these fluids in rhesus monkeys.

Animals↗
PubMed1976

Comparison of polymerized and unpolymerized antigen E for immunotherapy of ragweed allergy.

Polymerization of ragweed antigen into high-molecular-weight polymers could improve immunotherapy for ragweed pollinosis by reducing side effects while retaining immunogenicity. To study this thesis, 23 ragweed-sensitive patients were treated with either ordinary ragweed antigen E or ragweed antingen E polymerized by glutaraldehyde. Four patients received the polymerized antigen, and six controls ordinary antigen according to the standard immunotherapy schedule; two groups of three patients received either form by a "doubling-dose" schedule. Seven subjects received the polymerized antigen by a schedule in which each successive dose was tripled. Serum antigen E binding capacity (blocking antibody) increased significantly in all subjects (P less than 0.001 by Student-test). Patients treated with polymerized antigen had fewer local and generalized reactions than those receiving the monomeric preparation. Polymerized ragweed antigen permits more rapid immunization of atopic persons, with fewer side effects than standard monomeric preparations.

Adult↗
PubMed1975

The diisopropylfluorophosphate inhibitable step in antigen-induced histamine release from human leukocytes.

DFP inhibits early events in antigen-induced histamine release from human leukocytes. If added to cells 5 min or more after antigen it is ineffective. If added with antigen it can be removed at 5 min but release will still be inhibited. In contrast, ethylenediaminetetraacetate (EDTA) and 2 deoxyglucose (2DG) still inhibit the reactions when added 5 min after antigen. During incubation of leukocytes for 90 to 120 min at 0 degrees C they react with specific antigen since they subsequently release significant quantities of histamine after washing and reincubation at 37 degrees C without addition of antigen. Such priming at 0 degrees C is at least equivalent to priming for 2 to 4 min at 37 degrees C. During antigen priming at 0 degrees C the cells are not activated beyond the step in the release sequence which is inhibited by diisopropylfluorophosphate (DFP). This is apparent from the undiminished inhibitory activity of DFP on these cells. Furthermore, cells primed with antigen at 0 degrees C in the presence of DFP release as much histamine after washing and incubation at 37 degrees D as control cells primed in the absence of DFP. Incubation of leukocytes with specific antigen at 37 degrees C for 3 min resulted in significant but not quite complete priming for subsequent histamine release in the absence of antigen. Most of these primed cells were not activated beyond the step inhibitable by DFP. However, some had completed the entire sequence including the release of histamine while others had not released their histamine but were not inhibited by DFP from subsequent release. After 5 min incubation with antigen at 37 degrees C almost all leukocytes had progressed beyond the stage which is inhibited by DFP. Incubation of leukocytes at 37 degrees C with DFP but without antigen for up to 15 min followed by washing did not impair subsequent antigen-induced histamine release by these cells. Thus, DFP was inhibitory under these conditions only after antigen activation of leukocytes.

Antigens↗