Biomedical subjects
Publications and source records attributed to M Boris.
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Five subjects with a history of asthma after exposure to cat or dog underwent a trial of low-dose antigen injection followed by bronchoprovocation with the relevant antigen. The neutralization dose of antigen was determined by serial and point dilution skin testing. In a crossover protocol, patients received this antigen or placebo injections. They then underwent bronchoprovocation with the same antigen. The results of the early and late reaction to bronchoprovocation were compared, with each patient serving as her own control. As measured by the number of breath units to lower the FEV1 by 20%, placebo group tolerated only 6.9 +/- 2 breath units, whereas the neutralization group tolerated 29 +/- 3 breath units (p less than 0.05). The maximum decline in FEV1 during the late reaction was 27 +/- 13% after injection of placebo and 12 +/- 12% after injection of antigen (p less than 0.05). In this model of antigen-induced asthma, injection of low doses of allergen immediately preceding bronchoprovocation blunted the immediate and delayed asthmatic reaction.
Crohn's disease is a chronic inflammatory disorder for which an immunologic etiology has been proposed. Food hypersensitivity may contribute to part of the pathogenesis of this disorder. In preliminary studies, we evaluated 11 Crohn's patients by history, skin testing (ST), total and specific(s) IgE and sIgE/sIgG4 levels to five food proteins [egg (E), milk (M), wheat (W), soy (S), and corn (C)] using a sensitive enzyme monoclonal antibody assay. Skin testing was also performed using grass and mold allergens. Lymphocyte concanavalin (Con A) mitogenic and antigenic responses to food proteins were also determined by tritiated thymidine incorporation. Mean sIgG4 values for four food proteins are listed below: (Table: see text). No patient reacted with elevated sIgE or sIgG4 to corn. All patients had low to negative sIgE levels to all foods and only three had increased total IgE. Three of eight were history and ST positive to M, E, and W. Six of eight had at least one positive ST to M, E, W, and S. All patients had negative sIgG4 to tested inhalants and two had elevated sIgE to grass pollen. Although mean lymphocyte Con A mitogenesis was significantly decreased in eight patients compared with controls (P less than .05), an increased food stimulatory response to milk protein was observed (P less than .05). Perhaps, decreased sIgE and cell-mediated mitogenic responsiveness may lead to an enhanced humoral IgG response. The increased sIgG4 humoral response to egg protein and cellular sensitivity to milk protein may indicate mucosal antigenic stimulation or leakage in patients with Crohn's disease in spite of negative sIgE levels.
Injection of low-dose antigen on a co-seasonal basis has been proposed as an alternative to conventional immunotherapy in allergic disorders. Few studies of efficacy have been attempted, and available data do not support the use of this technique. We evaluated the effect of low-dose antigen injection in 21 subjects with histories of asthma, after exposure to animal antigen. Each subject was injected with low-dose animal antigen, as determined by skin test end point titration, or with placebo. Twenty minutes after the injection, bronchoprovocative challenge was performed with the use of the same antigen. The provocative dose 20% (PD20), FEV1 after antigen injection, was 28.52 +/- 1.74, was compared to 6.50 +/- 1.15 after placebo injection (p less than 0.01). This experiment was repeated after pretreatment of patients with indomethacin. The protective effect of antigen injection was abolished. In a third experiment, the PD20, FEV1 for methacholine, was 10.74 breath units (BU) after antigen injection and 6.84 BU after placebo injection (PD less than 0.05). Low-dose antigen injection causes rapid reduction of bronchial sensitivity to inhaled antigen and methacholine. This effect is abolished by treatment with indomethacin.
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During the course of studying the effect of normal nasal flora on the growth of L-forms, a clear zone of inhibition was observed around colonies of many coagulase-negative staphylococci. Subsequent investigation demonstrated that Staphylococcus aureus and some S. albus strains produce a substance which is capable of markedly inhibiting the growth of stable staphylococcal and streptococcal L-forms. This interfering substance is separable from the staphylococcal organism and is diffusible through 1.5% agar, but not through a dialysis membrane. It is heat-stable.
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