Search PubMed⌕ Search

Biomedical subjects

H Bazin

Publications and source records attributed to H Bazin.

At least 217 records · Page 12Linked to original sources
PubMed1983

Antigen-induced release of histamine from serosal mast cells, lung, and tracheal tissue: variation with tissue and rat strain in relation to serum IgE-antibody level.

Rats of the Brown Norway (BN)2, Fischer, PVG and Sprague Dawley (SD) strains were immunized intraperitoneally with graded doses of ovalbumin (OA) together with either alum or Silica gel. At specified times after immunization, in vitro histamine release from serosal mast cells and from chopped lung and tracheal tissue was determined after challenge with OA. The development of the capacity to respond in these tests seemed to vary within strain independently for mast cells, lung, and tracheal tissue with immunization dose of antigen and nature of adjuvant. These variations were not closely correlated to observed variations in serum levels of OA-IgE antibody or ratio OA-IgE to total IgE as determined by radioimmunoassay. Furthermore, variations between strains in response capacity did not correlate to inter strain variation in median serum OA-IgE antibody level. These results do not clearly conform to the possibility that one single class of IgE mediates anaphylactic reactivity of various tissues of the rat.

Animals↗
PubMed1983

Rat hybridoma technology: culturing of rat myeloma cell line IR983F prior to cell fusion.

The nonsecreting IR983F rat myeloma cell line grew exponentially with a mean generation time of 16 h when reset daily at 5 X 10(5) cells/ml in culture medium with horse serum. High yields of rat-rat hybrids were systematically obtained when fusing exponentially growing IR983F cells with syngeneic immune spleen cells. The yields of hybrids secreting specific antibodies varied greatly according to the immunisation procedure. In the best conditions, 22 hybrids secreting anti-human leukocyte antibodies were recovered per 10(7) plated cells.

Animals↗
PubMed1983

The non-specific enhancement of allergy. I. In vivo effects of Bordetella pertussis vaccine on IgE synthesis.

Bordetella pertussis organisms, with or without a small dose of alumhydroxide, enhance in rats the production of IgE antibodies to an unrelated antigen, even if this antigen has been administered 6 weeks beforehand. This non-specific enhancement of IgE antibodies is accompanied by a substantial rise in total serum IgE and by the production of IgE antibodies to B. pertussis. The effect of B. pertussis on IgE synthesis is dose-dependent. No effect of B. pertussis on IgE production can be observed in nude rats.

Adjuvants, Immunologic↗
PubMed1983

The non-specific enhancement of allergy. II. Precipitation of anaphylactic in vitro response capacity and serum IgE and IgG2a antibody synthesis in primed but non-responding rats by injection of alum.

PVG rats given injections of 1 microgram ovalbumin (OA) together with 10 mg Silica gel failed to provide serosal mast cells or lung tissue with the capacity to release histamine on in vitro challenge with the antigen. However, if such animals were injected i.p. with 100 mg of alum (without any further antigen addition) 3-9 weeks after the primary antigen injection, their mast cells and lung tissue showed a clear-cut capacity to respond in vitro, when examined 1 week after the alum injection. Injection of only 15 mg alum did not induce such a response capacity. The fading of the reactivity induced by an alum injection could be prevented by a repeated injection of the adjuvant alone. Pretreatment of the rats with cyclophosphamide (33 mg/kg) 2 days before the primary antigen injection did not affect the response capacity induced by a booster injection 3 weeks later. S.c. injection of alum also precipitated response capacity in animals primed by i.p. injection of antigen and Silica gel. The anaphylactic response capacity induced by injection(s) of alum was generally accompanied by increased levels of OA-IgE and especially OA-IgG2a antibody; however, a clear-cut correlation between either serosal mast cell or lung tissue response capacity and serum OA-IgE or IgG2a antibody titer could not be demonstrated. These data show that in primed animals, which do not express allergic response capacity, such a capacity can be induced by injecting adjuvant alone, even several weeks after the primary antigen injection.

Aluminum Hydroxide↗
PubMed1983

The non-specific enhancement of allergy. III. Precipitation of bronchial anaphylactic reactivity in primed rats by injection of alum or B. pertussis vaccine: relation of response capacity to IgE and IgG2a antibody levels.

SD rats were sensitized by an i.p. injection of 1 microgram or 10 micrograms ovalbumin (OA) together with 10 mg Silica gel. At the indicated time after sensitization, allergic response capacity of the animals was estimated by measuring changes in intratracheal pressure induced by an i.v. injection of 0.3 mg OA (low challenge dose) or 5 mg OA (high challenge dose). Animals given 1 microgram OA in Silica gel showed no response capacity at 14, 35 or 47-48 days after sensitization. Animals injected with 10 micrograms OA showed a clear-cut response with a peak at 14 days; at 7 weeks after immunization the response capacity had faded almost completely. Specific OA-IgE antibody and total IgE serum levels were examined by radioimmunoassay. A slight increase in OA-IgE antibody was recorded in animals injected 14 days before test with 10 micrograms ovalbumin and Silica gel; animals given 1 microgram OA and Silica showed no OA-IgE antibody. Five weeks after sensitization, some animals of each group were injected i.p. with 100 mg alum, B. pertussis vaccine (2 ml of Perthydral), or saline, all injections being made without any further antigen addition. 12-13 days after such an injection, alum-treated animals showed high response capacity at bronchial anaphylactic tests and high OA-IgE antibody levels but comparably low levels of total IgE. Animals injected with B. pertussis, on the other hand, showed low response capacity (bronchial anaphylactic tests and OA-IgE antibody levels) but high total IgE-antibody levels. The bronchial anaphylactic response in the B. pertussis-injected animals but not the alum-injected animals was significantly correlated to serum IgG2a antibody levels. These results show that injection of alum or B. pertussis vaccine without antigen can precipitate/enhance anaphylactic response capacity and production of specific and non-specific IgE and IgG2a.

Adjuvants, Immunologic↗
PubMed1983

Genetic regulation of immunoglobulin synthesis: selection of two rats' lines with respectively a high or low IgM serum level.

Two directional selections of rats for a high or a low IgM serum levels have been carried out. The criterium of selection was the individual merit of each rat in having a high or a low IgM level when they were 3 months old. All animals were kept together, in order to avoid external influence on the IgM synthesis. The founding population was a mixed nucleus of rats, obtained by breeding of 13 different strains of inbred or outbred rats for two generations. Two lines, one with a high IgM serum level and another with a low IgM serum level, have been separated. At generation 10, they differed from each other by a coefficient of approximately four. These IgM serum levels were not due to differences in IgM catabolism of the two lines since both lines had similar IgM half-lives. Analyses of the data obtained show that, for IgM synthesis, the coefficient of heritability varies between 0.30 to 0.40, and the number of 'independent loci' controlling IgM synthesis ranges from 11 to 14.

Animals↗
PubMed1983

Formation of biologically inactive polymers is responsible for the thermal inactivation of rat IgE.

The structural changes induced by heating rat IgE at 56 degrees C and relationship with loss of cytotropic activity were examinated in the present study. Circular dichroism spectrum of IgE heated at 56 degrees C showed irreversible changes in the peptide bond spectral regions: increase in beta-sheet structure, but no significant modifications in the aromatic side chain region. Thus, circular dichroism studies did not suggest important perturbations of the tertiary structure of the IgE molecule. Parallel studies with F(ab')2-epsilon fragment did not show significant alterations of either peptide bond or aromatic side chain spectral regions. Analysis of IgE heated at 56 degrees C by polyacrylamide gradient gel electrophoresis showed the presence of large amounts of polymeric material. Polymerization of IgE was found to increase with time of heating at 56 degrees C and to depend on protein concentration; polymerization was decreased at temperatures lower than 56 degrees C. A relationship between loss of cytotropic activity and the proportion of polymeric material in the heated IgE solutions was observed. Isolated polymeric molecules produced by heating showed considerable decrease in cytotropic activity whereas monomer isolated from heated IgE was found biologically active. The ability to form polymers is an intrinsic property of the carboxy-terminal domains C epsilon 3 and C epsilon 4, as the F(ab')2-epsilon fragment did not polymerize upon heating at 56 degrees C. A model of thermal inactivation of rat IgE is proposed in which aggregation of the carboxy-terminal domains of the epsilon-chain does not allow interaction of these domains with the monovalent IgE receptor of mast cells.

Animals↗
PubMed1983

Trypanosoma cruzi: variation in susceptibility of inbred strains of rats.

Eight strains of male rats (AUG, BN, LEW, LIS, WAG, F 344, LOU/M, DA) and 3 strains of female rats (LEW, F 344, KGH) were challenged with 15 X 10(4) trypomastigotes of the Tehuantepec strain of T. cruzi. Parasitemia and mortality were observed for 60 days. Varying degrees of susceptibility were demonstrated between strains: complete resistance (R), no parasitemia; low resistance (LR), mild parasitemia; and no resistance (NR), high parasitemia. The differences in susceptibility to T. cruzi, using inbred strains of rats, were unrelated to Rt-1 haplotype. However, the level of parasitemia and host survival are not necessarily related; both male and female F 344 hosts are susceptible (NR) to T. cruzi but only females survive.

Animals↗
PubMed1983

Obtention of rat monoclonal antibodies reactive with human leukaemic lymphoblasts.

The Louvain rat-rat hybridoma technology was used to analyse membrane antigens present on human leukaemic lymphoblasts. Three fusions directed against non T non B leukaemic lymphoblasts finally yielded 42 distinct, stable, and specific antibody-secreting hybridomas. The cellular and molecular specificities of these monoclonal antibodies are still under investigation. However, a striking feature of our preliminary characterization is the obtention, in single fusions, of several distinct hybridomas that secrete antibodies binding to the same membrane molecule.

Animals↗
PubMed1983

Antibody-dependent cellular cytotoxicity (K) and natural killing (NK) in B-suppressed germ-free nude rats.

The influence of the thymus and the possible requirement for surface immunoglobulin expression for the development of K and NK activity were assessed in rats. This species was chosen in preference to mice as they show good levels of K-cell activity. Studies were carried out in athymic (rnu/rnu) rats some of which were treated from birth with rabbit anti-rat IgM antibody to suppress B-cell development. The results indicate that normal levels of both K and NK activity develop in the spleens of 6-8-week-old athymic rats, which do not contain cells expressing surface membrane immunoglobulin. While K and NK cells show characteristics of the lymphoid lineage, neither the thymus nor surface membrane immunoglobulin expression appears to be required for development of normal levels of these cytolytic activities.

Animals↗
PubMed1983

Immunologic response of athymic rats to Schistosoma mansoni infection. II. Antibody-dependent mechanisms of resistance.

The responses of congenitally athymic rats to Schistosoma mansoni were compared to thymic reconstituted, heterozygous littermate controls, and inbred Fischer rats. The mechanisms of the impaired resistance of athymic rats to initial exposure and re-exposure to S. mansoni were investigated by the study of various parameters of antibody response. The uninfected athymic animals demonstrated normal levels of total IgM but reduced levels of total IgG2a and IgE. After infection with S. mansoni, the immunoglobulin increases in athymic rats were less than those observed in heterozygote control rats. In addition, the level of anti-S. mansoni IgG antibody, utilizing ELISA assay, was reduced. Furthermore, the functional avidity of the IgG2a antibody, which was produced by the athymic animals, was significantly lower than that of control heterozygote and Fischer animals. Similarly, the levels of IgE and IgG2a anaphylactic antibodies were reduced in the congenitally athymic animals. After thymic reconstitution and exposure to S. mansoni of the congenitally athymic animals, all of these parameters became similar to the analogous value obtained from exposed heterozygous and homozygous animals. In vitro studies of antibody-dependent cell-mediated cytotoxicity (ADCC) activity indicated that the antibody response of the congenitally athymic animals was characterized by significant reductions in IgE-macrophage-mediated, IgG-eosinophil-mediated, and IgE-eosinophil-mediated cytotoxicity directed against schistosomula. These results, coupled with previously reported in vivo observations, that athymic animals produced antibody that was less capable of transferring resistance in adoptive-challenge experiments, suggest that the mechanisms of impaired resistance in the congenitally athymic rat may involve the failure to develop adequate, functional ADCC mechanisms. As such, these studies suggest a relationship between in vivo resistance and possible in vitro mechanisms of that resistance.

Animals↗
PubMed1982

Non-random chromosomal changes involving chromosomes 6 and 7 in spontaneous rat immunocytomas.

G-banding analysis of seven Ig-secreting spontaneous rat immunocytomas showed a consistent translocation of the distal part of the q-arm of chromosome 7 to the telomeric end of chromosome 6. The breakpoints were assigned to q3.3 on chromosome 7 and q3.2 on chromosome 6. Previously, we found a similar translocation pattern in mouse plasmacytomas induced by different agents. The distal part of the q-arm of chromosome 15 was translocated to the telomeric end of chromosome 12, known to carry Igh, the immunoglobulin heavy chain cluster. The banding homologies between the chromosomes involved in the translocation in the two species suggest that a similar mechanism is responsible for plasmacytomagenesis in both. We also predict that the rat Ig heavy chain gene cluster will be located to the terminal segment of chromosome 6.

Animals↗
PubMed1982

Migrant mu+ delta+ and static mu+ delta- B lymphocyte subsets.

Immunoglobulin isotype expression in isolated lymph node (LN), spleen and blood lymphocyte suspensions was assessed in rats. The proportion of mu+ delta- B cells in spleen (34%) was approximately twice that in blood and LN. Immunohistological examination of spleens showed the cells of the marginal zones to be predominantly mu+ delta-. On the other hand, mu+ delta+ B cells were mainly confined to the follicles in both spleen and LN. These follicles had a minor mu+ delta- component. The migratory properties of B cells with these two phenotypes were assessed by depleting lymphocytes migrating through the white pulp of rat spleen. This was achieved by placing a 32P-impregnated beta-emitting polythene strip over one half of the spleen. Examination of the nonirradiated half of the spleen, LN and peripheral blood after 12 days irradiation showed selective loss of delta + B cells. The mu + delta- cells of the splenic marginal zone were numerically unaltered. There was also a substantial residual mu + delta- B cell presence in the small lymphocyte compartment of follicles of LN and spleen in depleted animals. In addition, the blood selectively retained a mu + delta- B cell component. This was not derived from the spleen, as mu + delta- blood B cell numbers were sustained even where both halves of the spleen were irradiated. It is concluded that: (a) the major static B cell component of spleen and LN is mu + delta-, (b) that most if not all delta + B cells repeatedly migrate through the spleen and (c) there is a blood-born mu + delta- component which is resistant to depletion by splenic irradiation.,

Animals↗