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Biomedical subjects

J Hébert

Publications and source records attributed to J Hébert.

At least 73 records · Page 4Linked to original sources
PubMed1988

Analysis of compound 48/80-induced skin histamine release and leukotriene production in chronic urticaria.

Profiles of histamine release by nonlesional skin mast cells from patients with chronic urticaria (CU) and normal control (NC) subjects were compared on stimulation with a wide range of concentrations of compound 48/80 (0.15 to 4.8 mg/ml). One previous observation demonstrating spontaneous and 48/80-induced release of histamine greater in patients with CU than in NC subjects was confirmed with a concentration of 48/80 believed to produce mast cell activation in most subjects (2.4 mg/ml). In fact, higher concentrations of histamine were released by patients with CU than by NC subjects on stimulation with 48/80 at concentration greater than 0.6 mg/ml. With 0.6 mg/ml of 48/80, the profiles of histamine release were comparable in the two groups, and for concentration less than 0.6 mg/ml, the profiles of release were completely different, being higher in NC subjects than in the group with CU. The peak histamine response was higher in the group of NC subjects (6500 pg/ml) than in the group with CU (5100 pg/ml), and the concentration of 48/80 needed to trigger maximum release was lower in the NC subjects than in the subjects with CU (0.15 versus 0.6 mg/ml). The production of leukotriene B4 and leukotriene C4 was also compared in these two groups after stimulation with 2.4 mg/ml of compound 48/80. No significant amount of leukotriene B4 was found in the collection chambers, but small amounts of leukotriene C4 were measured into skin chamber fluids during a period of 4 hours. No significant difference could then be observed between the two groups.

Adult↗
PubMed1988

Polyester arterial grafts impregnated with cross-linked albumin: the rate of degradation of the coating in vivo.

One of the techniques used to avoid preclotting a porous textile arterial prosthesis is to coat the graft with a layer of a bioerodible polymer. The efficacy of this treatment is dependent in part on the rate at which the polymer degrades after implantation. The focus of this study was therefore to investigate the rate of in vivo degradation of albumin-coated polyester (Dacron)-knitted vascular prostheses. Two types of cross-linked albumin were included: one using glutaraldehyde, the other using carbodiimide as the cross-linking agent. Radioactively labeled albumin-coated prostheses were implanted in the thoracic aorta and peritoneal cavity of dogs, and their rates of biodegradation in vivo were monitored over a 4-week period. The rate of biodegradation was found to depend upon the site of implantation. It occurred more rapidly in the peritoneal cavity where less than 20% of the albumin coating remained after 4 weeks in vivo in comparison to the approximately 30% in the thoracic aorta. The nature and intensity of the cellular response appeared to be related to the cytotoxic potential of the cross-linking agent. Glutaraldehyde induced an inflammatory response and a delay in healing, whereas carbodiimide caused only a mild tissue reaction.

Animals↗
PubMed1988

Demonstration of idiotypes expressed on basophil-bound IgE antibodies by using anti-idiotype-induced histamine release in grass pollen-allergic patients.

This study was designed to analyse further the idiotypic cross-reactivity between anti-Lol p I murine monoclonal antibodies of IgG isotype and basophil-bound human IgE antibodies from grass pollen-sensitive patients. It was also designed to determine the expression frequency of the idiotypes present on cell-bound IgE. Rabbit anti-idiotypic antisera were produced against idiotypes of three anti-Lol p I monoclonal antibodies (290A-167, 539A-6 and 348A-6) of different specificities. Basophils from 19 patients reacting to Lol p I allergen, as shown by positive skin test reactions and by the presence of serum-specific IgE antibodies (measured by RAST), were challenged with these rabbit anti-idiotypic antibodies and the histamine released was measured. Our data indicate that IgE-borne idiotypes were expressed as follows: (i) co-expression of the three idiotypes in 15% of patients; (ii) co-expression of two idiotypes in 21% of patients; and (iii) expression of a unique idiotype (290A-167) in 42% of patients. Among the three idiotypes, 290A-167 was shown to be a public idiotype since it was expressed in 80% of patients. Fab fragments of anti-idiotypic antibodies could inhibit anti-idiotype-induced histamine release, but optimal conditions varied from one patient to another.

Adult↗
PubMed1988

Characterization of anti-idiotypic antibodies and their use as probes for determination of shared idiotopes expressed on murine and human IgE anti-rye I antibodies.

This study describes the production and characterization of rabbit anti-idiotypic antibodies (anti-ID Abs) against three idiotypes of three mAbs with different specificities. The anti-ID Abs were rendered idiotype specific by appropriate adsorption. Binding of labelled mAb to homologous anti-ID Ab bound to a polystyrene matrix was completely inhibited when the same mAb was added. In contrast, addition of other mAbs sharing the same isotype and the same light chain but with different specificity did not affect the binding reaction. Each anti-ID Ab inhibited completely and selectively the reaction between the allergen and the homologous mAb idiotype. Labelled rye I binding to a given polystyrene-bound mAb idiotype was completely blocked if the relevant anti-ID Ab was used as an inhibitor. Murine polyclonal anti-rye I antisera inhibited the reaction between all three mAbs and the antigens, as well as the reaction between all three mAb idiotypes and their homologous anti-ID Abs. On another hand, goat polyclonal anti-rye I antisera only inhibited the reaction between the mAbs and the antigens. These results suggest that the anti-ID Abs produced are directed against idiotopes located within the paratopes and such idiotopes are shared by murine monoclonal and polyclonal Abs. Human rye I-specific IgE and murine anti-rye I mAbs could share common idiotopes, since human IgE binding to the antigen was inhibited by the anti-ID Abs. These observations imply structural similarity in the V gene coding for the variable region of the antibody of two different species.

Allergens↗
PubMed1987

Prevalence and characteristics of late asthmatic responses to exercise.

The prevalence and characteristics of late asthmatic responses to exercise were studied in an adult asthmatic population. Twenty-four subjects (eight male and 16 female), aged 17 to 39 years (mean, 23.7 years), performed a 6-minute exercise on a bicycle ergometer at 75% of their maximum oxygen intake. FEV1 was measured at regular time intervals up to 8 hours after exercise. Seven subjects demonstrated a late asthmatic reaction defined as a fall in FEV1 greater than 10% between 2 to 8 hours. Bronchial reactivity to histamine was unchanged 24 hours after the exercise, compared to baseline. On a control day, a fall in FEV1 similar to the one observed after exercise was induced by methacholine inhalation. Measurements of FEV1 were done at the same time intervals as on exercise day. Neutrophil chemotactic activity was measured in the serum of 15 subjects, on exercise day for early responders, and on the 3 test days for subjects with a dual response. There was no difference between subjects with an isolated early or late response for age, sex, or atopic status. Baseline expiratory flows and nonspecific bronchial reactivity to histamine were similar in both groups. These results demonstrate the occurrence of a late asthmatic response in 30.4% of the population studied. There was no significant change of nonspecific bronchial responsiveness after the late asthmatic response to exercise. No significant increase in neutrophil chemotactic activity could be observed.

Adolescent↗
PubMed1987

Suppression by relevant allergen of the spontaneous in vitro production of rye group I specific IgE antibodies by human peripheral blood lymphocytes.

The production in vitro of rye Group I specific IgE antibodies (rye I specific IgE Ab) by human peripheral blood lymphocytes (PBL) was examined. A sensitive enzyme-linked immunosorbent assay was developed which allowed the detection of rye I specific IgE Ab without interference from other immunoglobulin classes. A significant net synthesis of rye I specific IgE Ab by PBL from atopic subjects was detected only during the pollen season, which could not be observed with PBL from non-atopic donors whenever tested. This active synthesis in vitro of IgE antibodies by PBL from atopic patients in season was suppressed when PBL were pre-incubated with the relevant antigen. Furthermore, we are reporting data suggesting an inhibition of the passive release of preformed rye I specific IgE Ab from cells by the specific allergen.

Antibody Specificity↗
PubMed1986

Allergenicity and cross-reactivity of rye grass pollen extracts revealed by monoclonal antibodies.

Using monoclonal antibodies the immunogenic and allergenic characteristics of rye Group I were redefined by SDS-PAGE analysis and immunoblotting. The purified rye Group I from NIH possesses a major component of approximately 34000 Da against which most of the sera from grass-sensitive patients and none from non-atopic volunteers contain specific IgE antibodies. Monoclonal antibodies to rye Group I were raised and used to purify the antigen and to verify the cross-reactivity between grass extracts. The 3 monoclonal antibodies studied recognized different components of timothy grass and 2 of them recognized kentucky june grass but none recognized components of ragweed extracts.

Allergens↗
PubMed1986

Development of a reverse enzymoallergosorbent test (REAST) to detect timothy-specific IgE antibodies. Comparison with RAST.

Radioallergosorbent test (RAST) for the measurement of IgE antibodies has been introduced more than 15 years ago and a number of technical modifications have since improved its sensitivity and reproducibility. The test has been applied to the diagnosis of allergy and to determine changes in the levels of IgE antibodies following immunotherapy. However, specific IgG antibodies are raised during such a therapy and can interfere with the RAST. We have developed a reverse enzymoallergosorbent test (REAST) where microtiter plates are first coated with a purified polyclonal anti-IgE antibody, then with the serum to test and finally with peroxidase-labeled antigen. This assay is antigen specific as shown by the significant inhibition of binding of the labeled antigen in presence of unlabeled specific antigen (greater than 95%) and the absence of inhibition in presence of irrelevant antigens. The values found in atopic patients (85 subjects) were significantly higher than in the non-atopic donors (35 subjects) (1.14 U +/- 1.20 vs. 0.01 U +/- 0.02, P less than 0.0005) and there was a good correlation with the Pharmacia RAST (P less than 0.0005). The levels of specific IgE by both REAST and RAST correlated well with the clinical symptomatology.

Allergens↗
PubMed1986

Increased compound 48/80 induced local histamine release from nonlesional skin of patients with chronic urticaria.

Histamine released from skin mast cells in normal skin sites of patients with idiopathic chronic urticaria (CU) and normal volunteers was assessed with the skin chamber technique. Small amounts of histamine were spontaneously and continuously released during the 4-hour observation in both groups but were twofold greater in patients with CU. In addition, histamine levels were significantly more elevated in sites challenged with compound 48/80 than in unstimulated sites. Patients with CU differed from normal volunteers in that histamine release induced by 48/80 compound was significantly greater at 1 and 2 hours after challenge. The number of mast cells and the histamine content of the skin did not differ in the two groups. These observations could suggest a functional defect at the mast cell level rather than a difference in their numbers.

Adolescent↗
PubMed1986

Degradability of crosslinked albumin as an arterial polyester prosthesis coating in in vitro and in vivo rat studies.

In order to avoid the preclotting procedure in knitted polyester arterial prostheses and in woven models, compound polyester grafts have been proposed, containing preadsorbed collagen or albumin. Since we are currently investigating grafts impregnated with crosslinked albumin, it was decided to establish the degradation rate of this coating after stabilization with either glutaraldehyde (GA) or carbodiimide (CDI). Tests were performed in vitro by incubation in either PBS, plasma or pancreatin and in vivo by implantation in the abdominal cavity of rats. In PBS or plasma in vitro, the coatings were very stable (2% degradation after 144 h incubation), however, in pancreatin the CDI crosslinked albumin degraded much faster than the GA crosslinked albumin (more than 50% degradation in 12 h compared to less than 30% in 48 h). In vivo the degradation rates of the two types of crosslinked albumin were similar (almost all of the albumin having been lost after 4 weeks) but the cellular response was very different: a mild tissue reaction was observed with the CDI crosslinked coating whereas many foreign body giant cells were present on the GA crosslinked material.

Albumins↗
PubMed1986

Effects of H1 and H2 receptor agonists on nonspecific proliferative response of human peripheral blood lymphocytes.

Histamine is known to modulate immune responses through the induction of suppressor cell subsets. The inhibition studies with antagonists suggest that the H2 agonist accounts for most of the suppression. This work studies the effects of various concentrations of 3-methyl histamine (as negative control), histamine, and pure H1 (2-methyl histamine, 2-pyridyl ethylamine) and H2 (4-methyl histamine, dimaprit) receptor agonists on the mitogenic (phytohemagglutinin A) proliferative response of normal human lymphocytes. At high concentrations of agonists (10(-3), 10(-4) M) the suppression induced by the two types of agonists is comparable to that of histamine. At lower concentrations (10(-6) M) the suppression is seen only in the presence of the H2 agonist. The suppression induced by the two agonists is generally reversed in the presence of an H2 receptor antagonist. The H1 receptor antagonist did not abolish and even increased the suppression induced by histamine and the two agonists.

Cimetidine↗
PubMed1986

Human IgG and murine monoclonal antibodies share common idiotopes as determined by competitive binding to polystyrene and nitrocellulose-bound antigens.

Competitive binding to polystyrene-bound antigens showed that human rye Group I (rye I)-specific IgG recognize the same three distinct epitopes of rye I as three monoclonal antibodies directed against the same antigens. Anti-idiotypic antibodies against one of the monoclonal antibodies (290A-167) inhibit completely the reaction between rye I and the relevant monoclonal antibodies but do not affect the reaction between other monoclonal antibodies (348A-6 and 539A-6) and the antigens. Furthermore, rabbit anti-idiotypic antibodies produced against F(ab' )2 of human rye I-specific IgG could inhibit the reaction between two monoclonal antibodies (290A-167 and 539A-6) and the relevant antigens. Those results were obtained by competitive binding to polystyrene or to nitrocellulose-bound antigens. These data indicate a cross-reactivity of idiotypic determinants between human rye I-specific IgG and mouse monoclonal antibodies, which implies structural similarity in the V gene coding for the variable region of the antibody.

Animals↗
PubMed1986

Immunological and non-immunological release of leukotrienes and histamine from human nasal polyps.

Nasal polyps were obtained from 22 patients undergoing polyp surgery. They were chopped into fragments of approximately 2 mm2, washed free of blood, and passively sensitized with serum from timothy allergen sensitive patients (RAST 30-40%), then, challenged with timothy allergen. Analysis of the incubation medium after a 30 min challenge as assessed by reversed phase high performance liquid chromatography and bioassay revealed the presence of leukotriene (LT) LTB4, LTC4, LTD4 and LTE4 (29 +/- 9, 6.6 +/- 3, 62 +/- 13 & 86 +/- 23 pmol/g tissue wet weight, respectively). The human nasal polyps also released histamine which reached a maximum after approximately 5 min (2.8 +/- 1.28 nmol/g tissue), as measured by radioenzymatic assay. A similar profile of leukotrienes and histamine release was observed when the nasal polyps were stimulated with ionophore A23187. However, the ionophore stimulated release was greater than that observed for the antigen challenge. When human polyps were stimulated with a mixture of the ionophore and arachidonic acid, all the above products as well as 5-hydroxy-eicosatetraenoic acid (5-HETE), 12-HETE, and 15-HETE were detected in the medium. These data, taken together, demonstrate that human nasal polyps are able to release significant amounts of leukotrienes and histamine upon both immunological and non-immunological stimulations and that these responses might significantly contribute to the symptoms of allergic rhinitis.

Allergens↗
PubMed1986

[Comparison of 3 types of immunotherapy for treating grass pollen-induced allergic rhinitis].

Three modes of immunotherapy in the treatment of allergic rhinitis to grass pollen were compared in grass sensitive patients: aqueous extracts, alum precipitated extracts and alum adsorbed extracts from aqueous pyridine solution of grass pollens (Alavac G.). This study confirms the efficacy of therapy with aqueous extracts and alum precipitates where larger doses could be administrated in shorter courses. The clinical response of patients treated with Alavac G. was not significantly different from untreated patients during the 1984 season in spite of the fact that sp IgE antibodies were prevented to rise. The weak potency of these extracts was further confirmed by their inability to interfere with the measurement of sp IgE Ab levels by RAST, as opposed to the two other preparations. Therefore, in spite of a minimal clinical response and a weak potency of Alavac G, a multicenter trial with larger group of patients is needed before any firm conclusion could be made on this mode of desensitization.

Adolescent↗
PubMed1985

Effect of antigen stimulation on antigen-specific IgE-plaque-forming cells from peripheral-blood lymphocytes of atopics.

In the present study, it was shown that allergen challenge in vitro produced an increase in the number of antigen-specific IgE-plaque-forming cells of peripheral-blood lymphocytes from grass- or ragweed-allergic patients. Thus, the blood lymphocytes of all twelve (four rye grass I and eight AgE) sensitive donors responded whereas the blood lymphocytes of five non-atopic controls were unresponsive to antigen challenge. Allergen challenge doses of 10(-10)-10(-12) g/ml were found to give the greatest number of plaque-forming cells whereas the number of plaque-forming cells at challenging doses between 10(-9) and 10(-7) g/ml were either the same or less than those obtained with unchallenged cells. The results are discussed as to whether this in vitro model system represents in vivo response to allergen of the allergic patient.

Antibody-Producing Cells↗
PubMed1985

Detection of antigen-specific IgE-plaque-forming cells from peripheral-blood lymphocytes of ragweed- and grass-allergic patients.

The reverse haemolytic plaque assay was developed to measure antigen (AgE or rye grass I)-specific IgE-plaque-forming cells from the peripheral-blood lymphocytes of ragweed- and grass-allergic patients. The anti-IgE-developing antisera was shown to be isotype-specific, and the response of the assay was inhibited by 52% by the addition of 10 pg of antigen. In addition, the assay was shown to have a reproducibility (s.d.) of 15%. The blood lymphocytes from all fifteen atopic (grass and ragweed) patients were shown to form antigen-specific IgE-plaque-forming cells during the pollen season (mean value 115 cells) and up to 6 months after the season (mean value 56 cells). Cycloheximide appears to block the formation of the plaque-forming cells. This method appears to be sensitive and reproducible enough to study in vitro IgE antibody synthesis of peripheral-blood lymphocytes from atopics.

Antibody Specificity↗