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PubMedDate not supplied

Tolerance induction to an alloepitope involves antibodies interacting with the T cells activated by the alloepitope.

Hyperimmunization of BALB/c mothers with Ab1 (BALB/c anti-C57BL/6) antibody can alter the T-cell repertoire of the syngeneic offspring called BALB/c-p-Ab1. The latter are rendered tolerant to specific alloantigens and are therefore resistant to graft-versus-host disease (GVHD), when challenged 24-48 hours after birth with allogeneic spleen cells. These offspring appear to express cell structures recognized by hyperimmunized mothers and which are presumably the T-cell counterparts of Ab2. Our data suggest that tolerance induction in our mouse model may be modulated by an idiotype network acting during foetal life. The factor modifying the foetal cell repertoire is identified as Ab2 (BALB/c anti-Ab1) antibody transplacentally transmitted from mother to foetus, which seems to carry an "image" of the GVHD-inducing alloepitope and can induce a "GVHD-like" syndrome when passively injected intraperitoneally in normal BALB/c newborn mice.

Animals↗
PubMed1992

Hyperglycemic athymic nude mice: factors affecting in vitro insulin secretion.

The strain of athymic nude male mice (ANM) developed at the University of Southern California (USC) exhibits spontaneous hyperglycemia and relative hypoinsulinemia in vivo. To investigate factors that influence insulin secretion in this animal model of non-insulin-dependent diabetes mellitus, we utilized the isolated perfused mouse pancreas of the ANM-USC and control BALB/c mice. We compared in vitro glucose-induced insulin secretion in ANM-USC and control mice, inhibition of secretion by somatostatin, and variability of insulin secretion over the two-year period it took to complete these experiments. Glucose-induced insulin secretion from the isolated pancreas was biphasic in both ANM-USC and controls. Insulin secretion was quantitatively equal to or greater than control mice, depending on the phase of secretion analyzed and the source of the control mice. In contrast to pancreases of control mice, insulin secretion from ANM-USC pancreases was relatively resistant to inhibition of insulin secretion by somatostatin. Variability in insulin secretion over the two years in which these experiments were performed was greater from pancreases of control than that observed from pancreases of the ANM-USC. The hyperglycemic ANM-USC mouse does not demonstrate diminished insulin secretion in vitro yet is relatively hypoinsulinemic in vivo. Thus circulating factors other than somatostatin might contribute to the insulinopenic stage in this animal model.

Animals↗
PubMed1976

An experimental animal model for the study of human scirrhous carcinoma.

Scirrhous-like carcinomas were induced by the inoculation of cloned mouse mammary carcinoma cells into the cleared fat pads of BALB/c mice. The inoculated cells induced palpable tumors in 100% of the animals within 60 days. The epithelial cells in vivo grew in rows and clusters and were attached by short developing desmosomes. Microvilli and organelles were scarce; intracisternal type A particles were observed in all the epithelial cells. Carcinoma cells invaded the dermis and muscle. The stroma was formed by morphologically normal fibroblasts and large masses of collagen. No virus particles were observed budding from the epithelial cell surface or in the stromal fibroblasts. The similarities between the scirrhous-like carcinoma in BLAB/c mice and the juman scirrhous carcinoma suggest this animal system as a model for the study of the human disease.

Adenocarcinoma, Scirrhous↗
PubMed1992

Interactions between Trichomonas vaginalis and vaginal flora in a mouse model.

To study the role of vaginal flora and pH in the pathogenesis of Trichomonas vaginalis, an intravaginal mouse model of infection was established. By employing this model, the vaginal flora and pH of mice could be monitored for changes caused by the parasite. As a baseline, the endemic vaginal flora of BALB/c mice was examined first and found to consist mainly of Staphylococcus aureus and Enterococcus species (32-76%). Lactobacilli and enteric bacilli were moderate (16-32%) in their frequency of isolation, and the prevalence of both anaerobic species and coagulase-negative staphylococci was low (4-16%). Vaginal pH was recorded at 6.5 +/- 0.3. Estrogenization, which was required for a sustained T. vaginalis infection, did not significantly alter vaginal flora; however, a slight rise in the number of bacterial species isolated per mouse and a drop in vaginal pH (6.2 +/- 0.5) were observed. Trichomonas vaginalis-infected mice did not appear to show significant changes in vaginal flora although vaginal pH was slightly increased. This mouse model could have applications in both immunologic and pathogenic studies of T. vaginalis and, with further modifications, aid in the study of protist-bacterial interactions.

Animals↗
PubMed1979

Serum from infected mice suppresses macrophage-mediated immunity in Mycobacterium lepraemurium infection: a model for imparied macrophage immunity in human leprosy.

Differing patterns of Mycobacterium lepraemurium infection in inbred strains of mice are of interest as a model system for studying mycobacterial infections of man, e.g. M. leprae, which present with a spectrum of clinical disease. In vitro, macrophages from both resistant (C57B1) and susceptible (BALB/c) inbred strains of mice can be shown to be equally effective in controlling multiplication of M. lepraemurium. Experiments presented here show that in vivo, the potential mechanisms of macrophage-mediated immunity are suppressed in the susceptible (BALB/c) strain of mouse by a soluble factor(s) present in the serum and the peritoneal fluid of infected mice.

Animals↗
PubMed1976

Experimental myasthenia in Balb/c mice immunized with rat acetylcholine receptor from rat denervated muscle.

A new model of an autoimmune disease of the neuromuscular junction was obtained by injection of acetylcholine receptor purified from rat denervated muscles into Balb/c mice. Anti-rat, then anti-mouse acetylcholine receptor antibodies, appear in mouse serum during the immunization procedure. Electrophysiological investigations performed on immunized mice reveal a neuromuscular block similar to that found in myasthenia gravis. Not a single mouse with objective signs of muscular weakness was lacking anti-mouse acetylcholine receptor antibodies but no correlation was found between their level and the severity of the disease.

Action Potentials↗
PubMed1992

Modification of the amount of cholesterol in hepatic steatosis induced in susceptible and resistant mice infected with MHV3: a biochemical and ultrastructural study.

A mouse hepatitis virus-3 strain subcultured in our laboratory is a unique experimental model in which to study virus-induced liver steatosis. This strain produces massive lipid deposition not only in sensitive adult BALB/c mice but also (though less extensive) in virus-resistant adult A/J mice. Biochemical determinations have shown that this steatosis is characterized by an increased amount of neutral lipids (sterols and triglycerides) in infected livers of BALB/c mice and by a smaller increase in those of A/J mice. However, the relative percentage of cholesterol and triglycerides is similar in both strains. Liver phospholipid content was significantly decreased in both strains of mice. To discriminate between cytoplasmic and membrane cholesterol content in different types of liver cells, an ultrastructural study was performed with filipin, a specific cholesterol marker. This study shows on one hand an important increase in the cholesterol in the hepatocytes of BALB/c mice and a smaller increase in those of A/J mice, in agreement with biochemical data. However, marked cholesterol decrease and abnormal cholesterol distribution were observed in the endothelial liver cells of infected BALB/c mice. This decreased cholesterol content probably led to higher fluidity of these membranes, which could be related to the important drop in the number of endothelial cell fenestrae observed after mouse hepatitis virus-3 infection. Because in A/J infected mice neither a decrease in the amount and distribution of cholesterol nor decreased fenestration were observed in endothelial liver cells, these findings could be correlated with the resistance of these mice to the infection.

Animals↗
PubMedDate not supplied

Utility of beige mouse in leprosy research.

Dissemination of M. leprae to visceral organs is seen by four months onwards only in beige (C57BL/6/bgj) but not BALB/c mice following intravenous or intraperitoneal infections. Inoculation of the beige mouse derived M. leprae showed all the characteristics of M. leprae, including growth pattern in the foot-pads of BALB/c mice. M. leprae inoculated into foot-pads of beige mice multiplied faster than those in the foot-pads of BALB/c mice. The possibility of using beige mouse in chemotherapeutic studies in leprosy is discussed.

Animals↗
PubMed2026

Construction and evaluation of an independently generated transgenic mouse model carrying mutated human HRAS genes for short-term carcinogenicity assessment.

The study aimed to construct and evaluate an independently generated transgenic mouse model applied to the short-term carcinogenicity assessment. Mutated human HRAS fragment containing an intron point-mutation was inserted into C57BL/6JGpt mice via bacterial artificial chromosome transgenic technology, eventually generating BALB/c;B6J-Tg(hHRAS)16/Gpt mice, abbreviated as HRAS mice. The inserted human HRAS fragment in HRAS mice was characterized, revealing five tandem copies at chromosome 19. Baseline profiles, including biochemical, hematological, immunophenotypic, survival, and carcinogenic data of HRAS mice, were collected. To evaluate the tumor susceptibility in HRAS mice, we applied N-Nitroso-N-methylurea (MNU) to HRAS mice in a short-term carcinogenicity assessment conducted according to Good Laboratory Practice. The genetic characteristics of HRAS mice include five tandem arrays of mutated human HRAS fragments located in genomic coordinate 7,755,606 on chromosome 19 and the duplication of a 9-kilobase genome sequence (genomic coordinate 7,755,606-7,746,509) located on chromosome 19. HRAS mice showed a relatively lower incidence and range of spontaneous tumor formation during long-term observation compared to CByB6F1-Tg(HRAS)2Jic (Tg.rasH2) transgenic mice. The short-term carcinogenicity assessment showed a strong tumor response to MNU, with high incidences of lymphoma (≥ 90%) and stomach squamous cell papilloma (≥ 90%) in both male and female HRAS mice. The HRAS mice showed susceptibility to MNU and exhibited baseline characteristics distinct from those of Tg.rasH2 mice. The co-expression of HRAS and MKI67 at the cellular localization level was found in neoplasms of HRAS mice. These findings preliminarily evaluated the feasibility of HRAS mice applied to the short-term carcinogenicity assessment.

Animals↗
PubMed1979

[Functional activity of the lymphocytes of mouse lymph nodes in a system of viral carcinogenesis].

A study was made of the PHA-induced lymphocyte blastransformation (BT), and lymphocyte antitumor activity, using a model of progressive and regressive neoplastic process induced by the Moloney virus in mice BALB/c. The antitumor acitvity of lymphocytes was estimated by their ability to inhibit spheroid production by tumor cells. A lymphocyte BT and their antitumor activity was registered during a progressive growth of the tumor and its restoration as the tumor is regressing.

Animals↗
PubMed1992

The heart and antiphospholipid antibodies in MRL-lpr/lpr mice.

Our objective in this study was to determine possible associations between antiphospholipid antibodies (aPL) and histologically defined heart valve lesions in the MRL-lpr/lpr mouse, a suitable model for the antiphospholipid syndrome (APS). At monthly intervals, from 2 to 6 months of age, three MRL-lpr/lpr mice (two with anticardiolipin antibodies, one without) and two sex- and age-matched Balb/c mice (controls) were sacrificed for histological studies. Serum binding to phospholipids and DNA was studied at this time. We found thickened heart valves in 68% of MRL-lpr/lpr mice and in 80% of Balb/c mice, and no association with any of the antibodies tested was found. No evidence of coronary vasculitis or thrombi was found in any of the mice studied. Platelet counts in MRL-lpr/lpr mice were significantly lower (640.550 +/- 211.818 x 10(6)/ml) than in Balb/c mice (780.0 + 112.5 x 10(6)/ml) (p < 0.05), and no association was found between platelet counts and aPL. In this model of murine APS, aPL bear no importance in heart valve pathology.

Animals↗
PubMed1975

Genetic control of oncogenesis by murine sarcoma virus Moloney pseudotype. II. A dominant epistatic susceptibility gene.

We have shown in the preceding paper that AKR mice are highly resistant to M-MSV tumor development, and that resistance is transmitted as a dominant character. In the present studies the tumor-response pattern of F1 hybrids between resistant AKR and susceptible strains (C57Bl/6, BALB/c and B10BR) following injection with Moloney mouse sarcoma virus (M-MSV) resembles that of the non-AKR parent. Segregation is observed in first backcross (Bc1) and F2 mice, and the segregation ratios up to Bc3 mice fit a one-gene model. The data of triple cross hybrids suggests that this dominant susceptibility gene inhibits the phenotypic expression of M-MSV tumor resistance in some susceptible Fv1bb strains as well as in their hybrids with AKR. Neither Fv-1 nor H-2 exerts any significant influence on this complex system.

Animals↗
PubMed1975

An experimental model for evaluation of factors in tumor escape from immunological attack.

A model system is presented for studying the factors involved in tumor immunity. The initial observations with this system concern the importance of dose and route of administration of tumor cells on tumor growth. The data show that myeloma tumor cells, when inoculated i.v.in relatively large numbers, are eradicated by the immune response of an allogeneic host; tumor cells administered i.v. in smaller number escape from immune attack even though the host has the potential to mount an immune response. BALB/c mouse myeloma cells (MOPC-21) were transplanted s.c., i.p., or i.v. into H-2-compatible allogeneic DBA/ 2 mice. There was a marked difference in the response of the host to tumor given s.c. or i.p. as compared to tumor given i.v. Thus s.c. or i.p. inoculation resulted in lethal tumor growth when 5 x 10-3 or more tumor cells were given. In contrast, the outcome of i.v. inoculation depended on tumor cell dose. Although small cell doses ( 5x 10-4 down to 10-2) resulted in lethal tumor gosulted in lethal tumor growth with only 10% survival, large cell doses (10-5 to 5 x 10-7) resulted in tumor rejection and 70% survival. DBA/2 mice possess the immunological ability to react agaist the tumor when large doses of tumor cells (10-7) are given i.v. or i.p., since spleen cells obtained from such mice were found to be able to suppress the growth of MOPC-21 when a mixture of spleen cells and tumor cells was inoculated. On the basis of these initial observations, our model appears to relate especially to the idea that, in autochithonous tumor development or in metastasis of tumor, a small number of antigenic tumor cells, perhaps even a single cell, usually grows into a frank tumor in spite of the immunological competence od the host to respond to the tumor cells.

Animals↗
PubMed1992

In vivo efficacy of B43 (anti-CD19)-pokeweed antiviral protein immunotoxin against BCL-1 murine B-cell leukemia.

We show that a highly aggressive subclone of murine BCL-1 B-lineage leukemia expresses a single 2.4-kb transcript hybridizing to the human CD19 cDNA probe and reacts strongly with the anti-human CD19 monoclonal antibodies (MoAb) B43, B4, Leu-12, and J3-119. In contrast to their strong reactivity with anti-human CD19 MoAb, BCL-1 cells show no reactivity with MoAb directed against human CD22, CD72, HLA-DR, IgD, or IgM. Western blot analysis of BCL-1 whole cell lysates with the anti-human CD19 MoAb J3-119 showed a single 69-Kd protein band, which was not detected by the negative control MoAb G19.4 (anti-CD3). In contrast to BCL-1 cells, normal BALB/c splenocytes or mouse splenocyte/myeloma hybridoma cell lines did not (1) express any transcripts that hybridized to the human CD19 cDNA probe, (2) react with B43/anti-CD19 MoAb, or (3) express the 69-Kd protein that reacts with the anti-human CD19 MoAb J3-119. Murine BCL-1 B-cell leukemia thus provides a unique model of disseminated B-lineage leukemia to evaluate the antileukemic efficacy of anti-CD19 immunotoxins. This model was subsequently used to evaluate the in vivo homing ability, pharmacokinetics, and antileukemic efficacy of B43 MoAb conjugated to the plant hemitoxin pokeweed antiviral protein (PAP). B43-PAP immunotoxin (1) showed strong and antigen-specific reactivity with BCL-1 cells, (2) promptly penetrated the spleens of leukemic mice, (3) rapidly reduced the BCL-1 leukemia burden of leukemic mice and, most importantly, (4) improved survival. Finally, B43-PAP immunotoxin was more effective against BCL-1 leukemia than 700 cGy (LD100/30) total body irradiation (TBI) followed by syngeneic bone marrow transplantation (BMT).

Animals↗
PubMed1979

Selective polymyositis inducted by coxsackievirus B1 in mice.

A high-passage laboratory strain of coxsackievirus B1 produced a unique myositis that predominantly and profoundly affected hip extensors and, to a lesser extent, hindquarter knee flexors when inoculated into a strain of random-bred newborn mice of Swiss origin (COH mice). The effect was not observed in BALB/c or C3H mice similarly inoculated. In addition to the differences in susceptibility of the mouse strains, it was found that six different low-passage "field" isolates of coxsackie-virus B1 isolated from infected patients varied considerably in their capability to induce these lesions. Thus, selective myositis which is muscle group-specific can be induced in a mouse model with coxsackievirus B1, and both genetic factors of the host and characteristics of the virus strain play a significant role in the pathogenesis of the myositis.

Animals↗
PubMed1992

The virulence plasmid does not contribute to growth of Salmonella in cultured murine macrophages.

The virulence plasmid, characteristic of many serovars of Salmonella sp., and specifically its spv genes, promote intracellular growth of the bacteria in the liver and spleen and are essential for the virulence of these Salmonella serovars in the mouse. In an attempt to establish an in vitro model for studying its function, we evaluated its effect on the intracellular growth of the bacteria in macrophages in culture. We used a number of different macrophage-like cell lines (J774-A.1, IC-21 and PU5-1.8), as well as peritoneal or splenic macrophages from genetically Salmonella-sensitive (Itys, BALB/c) or resistant (Ityr, C3H/HeN) mice, and at different states of activation, stimulated in vivo or in vitro with lipopolysaccharide and/or recombinant gamma interferon. These were found to differ in their ability to suppress or sustain intracellular growth of several Salmonella serovars, but in all cases the growth was independent of the spv genes.

Animals↗
PubMed1976

Immunity to Plasmodium Berghei yoelii in mice. I. The course of infection in T cell and B cell deficient mice.

The course of infection with 17X nonlethal Plasmodium berghei yoelii was examined in BALB/c mice which were deficient in either T cells or B cells. Markedly increased parasitemia and mortality were observed in athymic (nude) mice which had been backcrossed on a BALB/c background (T cell deficient) compared to similar mice which had been grafted with neonatal BALB/c thymus, and were also observed in BALB/c mice suppressed from birth with goat antiserum to mouse mu-chain (B cell deficient) compared to age- and sex-matched BALB/c controls. These results establish the requirement for the presence of both T cells and B cells for effective resistance to an intercurrent infection with 17XNL P.b. yoelii in adult BALB/c mice. Mechanisms by which the requirement for both T cells and B cells could be explained were discussed. The model of mu suppression was shown to be a valuable tool for an evaluation of the cellular basis of immunity to an infectious disease.

Animals↗