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A Forget

Publications and source records attributed to A Forget.

At least 37 records · Page 2Linked to original sources
PubMed1985

Evolution of cell types and T-cell subsets in the spleens of Mycobacterium bovis BCG-resistant and M. bovis BCG-susceptible strains of mice after infection with M. bovis BCG.

In mice, the early host response to intravenous infection with small doses of dispersed Mycobacterium bovis BCG is controlled by the Bcg gene. After infection with a low dose of M. bovis BCG, Lyt-1+ cells were generated in the spleens of BCG-susceptible mice (Bcgs) in parallel with an increase in the proportion of phagocytic cells. Very few changes occurred in the splenic cell types of BCG-resistant mice (Bcgr).

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PubMed1985

Cellular immune response to Mycobacterium bovis (BCG) in genetically-susceptible and resistant congenic mouse strains.

Congenic Bcgr (C.D2, resistant) and Bcgs (BALB/c, susceptible) mice were infected intravenously with Mycobacterium bovis (BCG, strain Montreal) in order to establish the relationship between different indicators of the cell-mediated immune response and the bacterial load attained in the host. There was a correlation between the bacterial burden and the splenomegaly response, granuloma formation in the liver and cross-protection against an heterologous pathogen (Listeria monocytogenes) in Bcgr and Bcgs mice. No relationship was found between bacterial load or granuloma formation and the development of specific acquired protection against an homologous organism (BCG or M. tuberculosis, H37Rv) as assessed by the level of resistance attained in BCG-primed mice challenged with virulent H37Rv or by the adoptive immunity conferred by BCG-primed spleen cells transferred to naïve irradiated recipients challenged with BCG.

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PubMed1984

Regulation of resistance to leprosy by chromosome 1 locus in the mouse.

Mice of different inbred strains vary in their resistance to intravenous infection with Mycobacterium lepraemurium (MLM). The mean survival time of MLM-infected A/J and DBA/2 mice is significantly longer than that of similarly infected C57BL/6 and BALB/c mice. The typing of AXB/BXA recombinant inbred strains (A = A/J,B = C57BL/6) for the trait of relative resistance/susceptibility to MLM revealed a perfect match with the strain distribution pattern of resistance/susceptibility to Mycobacterium bovis (BCG), the trait which is controlled by the Bcg (Ity, Lsh) locus on chromosome 1. The control, by this gene, of response to MLM was further confirmed by the demonstration that BALB/c-Bcgr congenic mice, which carry the DBA/2-derived Bcgr (resistant) allele on chromosome 1, are significantly more resistant to MLM infection than their BALB/c (Bcgs, susceptible) counterparts.

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PubMed1984

Histological and immunopathological studies of delayed hypersensitivity reaction to tuberculin in mice.

At 4 to 6 weeks after intravenous infection with 2 X 10(4) CFU of dispersed Mycobacterium bovis bacilli (BCG), C3H/HeNCrIBR and C57BL/6NCrIBR mice exhibited a strong reaction to purified protein derivatives, as evaluated by the increase in footpad swelling at both 24 and 48 h after local antigenic challenge. However, histological studies of the footpad skin demonstrated a prominent perivascular infiltration with polymorphonuclear cells at 6 and 24 h after purified protein derivative challenge, whereas mononuclear cells represented the majority of infiltrating cells only at 48 h. An immunopathological study of the footpad skin showed granular deposits of immunoglobulins and complement in vascular walls and perivascular tissues at 6 and 24 h. These results demonstrate that the footpad swelling observed 24 h after the antigenic challenge is caused by an Arthus-type reaction, whereas that caused by cell-mediated immunity appears at 48 h. Hence, delayed hypersensitivity must be evaluated at 48 and not 24 h after challenge.

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PubMed1984

Phenotypic expression of genetically-controlled natural resistance to Mycobacterium bovis (BCG).

Mycobacterium bovis (BCG), when maintained in vitro, readily incorporates [3H]uracil, the RNA precursor. The rate of [3H]uracil incorporation into bacilli is sharply reduced when the BCG is phagocytized by murine adherent resident peritoneal macrophages and subsequently released by the lysis of monolayers. Macrophages derived from mouse strains that are innately resistant to BCG infection in vivo (Bcgr) are able to inhibit the [3H]uracil incorporation into the bacilli in a significantly more effective way than macrophages from BCG-susceptible (Bcgs) strains. This difference is best demonstrated with a low rate of infection (BCG: macrophage ratio between 1:1 and 2:1), and is most pronounced at 4 to 5 days after in vitro infection of macrophage monolayers. In vivo interaction of BCG with peritoneal macrophages in situ results in the same pattern of enhanced inhibition of [3H]uracil incorporation by Bcgr macrophages. The use of Bcg-congenic mouse strains has confirmed that the Chromosome 1 Bcg (Ity, Lsh) locus is regulating the antimycobacterial activity of macrophages. We conclude that the resident macrophage is the cell population that expresses the phenotype of genetically determined resistance to BCG infection.

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PubMed1983

A BALB/c congenic strain of mice that carries a genetic locus (Ityr) controlling resistance to intracellular parasites.

BALB/c.DBA/2 Idh-1b-Ityr-Pep-3b congenic mice were developed by introgressively backcrossing the Idh-1b and Pep-3b markers of DBA/2 mice onto the BALB/c pi mice. This introduced a 30-centimorgan chromosome 1 segment of DBA/2 chromatin that contained the Ityr gene. BALB/c.DBA/2 Idh-1b-Ityr-Pep-3b mice were resistant to in vivo infections by Salmonella typhimurium, Mycobacterium bovis, and Leishmania donovani.

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PubMed1983

Cutaneous unresponsiveness to Mycobacterium bovis BCG in intravenously infected mice.

Mice injected with 1 mg (about 1 X 10(7) CFU) of Mycobacterium bovis BCG in the footpad showed high levels of delayed-type hypersensitivity (DTH) to BCG antigens and a continuous increase in circulating specific anti-immunoglobulin G (IgG) antibodies throughout a 6-week observation period. In contrast, mice injected intravenously with a 1-mg dose failed to mount a DTH and showed a depression in antibody production at week 5 postinfection. A dose-response study revealed that an optimum dose of BCG, when injected intravenously, can induce a small but significant DTH response. The delayed cutaneous unresponsiveness in intravenously infected mice lasted at least 6 weeks and was not antigenically specific, in that it depressed the DTH response to Corynebacterium parvum. No simple relationship existed between levels of DTH and the amount of circulating anti-IgG antibodies. Splenectomy and treatment with a high dose of cyclophosphamide before infection, although greatly reducing the humoral response, did not reverse the BCG-induced unresponsiveness nor enhance levels of DTH in mice infected in the footpad. It is concluded that the intravenous infection of mice with BCG exerts a nonspecific inhibitory effect on delayed-type immune reactions by the induction of some type of suppressor mechanisms that are resistant to cyclophosphamide.

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PubMed1983

Cellular mechanisms of genetically controlled host resistance to Mycobacterium bovis (BCG).

Multiplication of Mycobacterium bovis (BCG) in the reticuloendothelial tissues of the mouse is controlled by the Chromosome 1 locus (Bcg), which exists in two allelic forms, resistant (Bcgr) and susceptible (Bcgs). We have investigated the phenotypic expression of this locus at the cellular level in vivo. No significant differences were observed in the early clearance of BCG from the bloodstream and peritoneal cavity, nor in the uptake of the infectious inoculum in spleen and liver of the mice of Bcgr and Bcgs strains. Inflammatory response to an i.p. injection of live BCG, with respect to both the cell populations involved and the kinetics of their appearance, was comparable in Bcgr and Bcgs mice. A kinetic study of BCG infection in congenitally athymic mice that carried the "nude" mutation on Bcgr (AKR/J) or Bcgs (BALB/c) background showed that the functional absence of T lymphocytes did not influence the expression of the Bcg gene. The population expressing the Bcg gene seems to be a mature cell of the mononuclear phagocyte lineage: it was resistant to a 950-rad dose of x-irradiation; it was susceptible to a prolonged exposure to silica; and, as demonstrated in radiation chimeras, it originated from bone marrow-derived precursors.

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PubMed1983

Immunosuppression during Trypanosoma musculi infection in inbred strains of mice.

Inbred strains of mice inoculated with T. musculi behaved as either sensitive (A/J, CBA/J and C3H/He/J) or relatively resistant (BALB/c, DBA/2, and C57B1/6) with respect to the magnitude of parasitaemia but not to the length of infection. Spleen cells from T. musculi infected C57B1/6 (resistant) and C3H/HeJ (sensitive) mice inhibited the response of normal spleen cells to PHA and ConA; this suppressive activity was concentrated in T-cells and was higher in the resistant mice. However, infection in T-cell-deprived C57B1/6 and C3H/HeJ mice, although more severe and of much longer duration than in the respective control mice, revealed that T-cells were not responsible for the natural resistance to T. musculi.

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PubMed1982

Immunopathology of BCG infection in genetically resistant and susceptible mouse strains.

Natural resistance to Mycobacterium bovis (BCG) is under the control of a single gene, designated Bcg. Resistant (Bcgr) mice prevent multiplication of an i.v. injected inoculum of congruent to 10(4) dispersed BCG cells, whereas progressive multiplication of this pathogen occurs in the first 3 wk of infection in spleens and livers of susceptible (Bcgs) mice. Striking differences in the development of cellular immunity, as measured by granuloma formation in the liver and spleen, delayed-typed hypersensitivity, and a resistance to the challenge with homologous (BCG) and heterologous (Listeria monocytogenes) pathogens, were detected between Bcgr (C3H/HeN and A/J) and Bcgs (C57BL/6J and B10.A) strains. Cellular immune reactions progressively developed in the Bcgs mice, as a response to the increasing bacterial load, whereas greatly inferior levels of acquired immunity were observed in Bcgr strains. These findings support the concept that mice genetically resistant to BCG infection are able to prevent bacterial multiplication without the need for a cellular immune response, whereas genetically susceptible mice will eventually control bacterial multiplication with the acquisition of cellular immunity.

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PubMed1981

Differences in response among inbred mouse strains to infection with small doses of Mycobacterium bovis BCG.

Intravenous infection of six inbred mouse strains with small doses of dispersed cells of Mycobacterium bovis BCG (15.5 x 10(3) or 15.5 x 10(4) colony-forming units) separated them into resistant (C3H/HeCr, A/J, and DBA/2) and sensitive (B10.A, C57BL/6, and BALB/c) strains as assessed by the magnitude of bacterial multiplication in the spleens at 28 days. The two groups were more sharply separated after infection with the lower dose of BCG (15.5 x 10(3) colony-forming units), which allowed for true multiplication of the bacteria in the spleens of permissive hosts, expressed as the ratio of the number of BCG recovered from the spleens to the number of BCG injected. This coefficient of increase was less than 1 in resistant strains, whereas it was higher than 2.5 in sensitive strains. Significant splenomegaly developed only in mice of the sensitive strains infected with BCG when compared with uninfected controls. There was no correlation between the magnitude of the delayed-type hypersensitivity (DTH) to BCG and susceptibility to infection: DTH was absent in both the sensitive and the resistant strains when the smaller dose of BCG was used for infection. Moreover, significant DTH was detected in animals of the most sensitive (BALB/c) as well as of the most resistant (C3H/HeCr) strain when the higher dose of BCG (15.5 x 10(4)) was used for immunization. These results document significant genetic differences in the ability of inbred mice to inhibit bacterial multiplication after infection with small dispersed doses of BCG. Resistance to BCG multiplication, in this model, does not appear to be related to the establishment of DTH.

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PubMed1981

Genetic control of natural resistance to Mycobacterium bovis (BCG) in mice.

Mice of 12 inbred strains infected i.v. with Mycobacterium bovis (BCG) exhibited 2 distinct patterns of response as determined by the degree of BCG burden in the spleens of animals at 3 wk after infection with 10(4) viable bacilli: susceptible (C57BL/6J and related sublines, BALB/c and DBA/1J) and resistant (A/J, C3H/HeCr, DBA/2J, CBA/J, C57Br, AKR). Mendelian analysis of this trait on segregating backcross and F2 populations derived from the mating of resistant and susceptible progenitors was compatible with the hypothesis that resistance to BCG is controlled by a single, dominant, autosomal gene, which is being given the designation Bcg. The product of the Bcg gene was found to influence the early phase of host response resulting in the genetic advantage of the resistant host being demonstrable as early as 24 hr after infection.

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PubMed1980

Modulating effect of passive immunization with anti-Mycobacterium tuberculosis antibodies on humoral response in BCG-infected mice.

Previous work has shown that the passive immunization with rabbit anti-Mycobacterium tuberculosis H37Rv antiserum of Mycobacterium bovis BCG-infected mice promotes the growth of bacilli in their spleen and induces a late production of antimycobacterial antibodies in their serum. The effect of the passive immunization on the early antibody response in infected mice has now been investigated. It was found that passive immunization with H37Rv antiserum of BCG-infected mice depressed the early humoral response as determined by the plaque-forming cell response to BCG extract when compared with BCG-infected mice treated with the antiserum freed from its mycobacterial antibodies as controls. In the BCG-infected mice treated with the rabbit antiserum freed from mycobacterial antibodies or treated with saline, the antibodies were present in the serum as soluble immune complexes which reached a peak 4 days after infection. These immune complexes were formed with mice antimycobacterial antibodies as determined with an antimouse immunoglobulin serum in the double diffusion test. On the other hand, in BCG-infected mice passively immunized with rabbit antimycobacterial serum, the immune complexes detected were mainly composed of transfer rabbit antimycobacterial antibodies as established with an antirabbit immunoglobulin serm. Comparison of the biphasic humoral response in passively-enhanced mycobacterial infection and allotransplanted normal tissue in the host is discussed.

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PubMed1977

An immunological enhancement phenomenon in experimental brucella infection of the chicks.

The passive transfer of chicken anti-brucella immune globulins promote the survival of Brucella abortus in the spleen of chickens infected with this bacteria. This enhancing effect was reduced significantly when the immune globulins were absorbed with heat-killed brucella cells to remove all the anti-brucella agglutinins and immune adherence antibodies. Therefore, it is most probable that the enhancing effect is related to the presence of brucella antibodies.

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PubMed1977

Enhancement activity of anti-brucella sera in experimental Brucella abortus infection in mice.

The passive transfer of rabbit anti-brucella sera promotes the multiplication of Brucella abortus in the spleen of mice infected intravenously with a low dose of this bacteria. The enhancement activity of the anti-brucella sera is related to their modes of preparation in rabbits. The agglutinin titers of all these antisera were relatively high, while there was some discrepancies in their content in haemagglutinating, immune adherence and complement fixing antibodies.

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PubMed1976

Enhancement activity of anti-mycobacterial sera in experimental Mycobacterium bovis (BCG) infection in mice.

The passive transfer of rabbit anti-mycobacterial immunoglobulins was directed against either living or soluble extracts of Mycobacterium tuberculosis strain H37Rv, which promotes the multiplication of the BCG strain of M. tuberculosis in the spleen of mice infected with low doses of this latter strain. This enhancing effect was reduced significantly when antisera were absorbed with living BCG. Moreover, such treatment led to the removal of all hemagglutinating antibodies when antisera were tested against either BCG or H37Rv soluble extracts. Therefore, it is most probable that the enhancing effect is related to the presence of mycobacterial antibodies.

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