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At least 127 records · Page 7Linked to original sources
PubMed1995

A mouse model for testing the pathogenicity of equine herpes virus-1 strains.

A mouse model was developed for testing the pathogenicity of equine herpes virus-1 (EHV-1) strains. The model was validated with EHV-1 strains that are known to be of a low or high pathogenicity in horses. From all parameters tested, the safety index, which was calculated from the body weights of the mice after infection, proved to be the best predictive parameter. When this parameter was used, good and reliable correlations were found with the pathogenicity of the EHV-1 strains in horses. This method enabled the differentiation between the two experimental EHV-1 strains whose genetic backgrounds were supposedly equal.

Animals↗
PubMed1987

A mouse model of chronic pulmonary infection with Pseudomonas aeruginosa and Pseudomonas cepacia.

A mouse model of chronic pulmonary infection with either Pseudomonas aeruginosa or Pseudomonas cepacia was developed to compare bacteriologic and pathologic features of these infections. Experimental pneumonia was established in Swiss mice by transoral intratracheal inoculation of 10(3)-10(4) colony-forming units of mucoid P. aeruginosa or P. cepacia enmeshed in agarose beads. Unilateral infection with either strain was tolerated without morbidity. By 10 days postinoculation, the mean colony-forming units per infected lung was 3.8 X 10(5) for P. aeruginosa and 1.0 X 10(5) for P. cepacia. Bacterial counts remained stable through 21 days with no significant difference between organisms. Acute and chronic inflammatory histopathologic changes similar to many found in the lungs of cystic fibrosis patients were present in 95% of lung specimens. The changes occurred with both organisms but were more extensive with mucoid P. aeruginosa. This model represents an important tool for study of the contribution of complement, antibody, and adoptive transfer of T cell-mediated immunity to the pathogenesis of chronic pneumonia with Pseudomonas species, and represents the first successful model of chronic pulmonary infection with P. cepacia.

Animals↗
PubMed1987

Hepatic lipid abnormalities in a chemical/viral mouse model for Reye's syndrome.

We have examined hepatic lipid profiles in a mouse model for Reye's Syndrome (RS) in which young animals are exposed to nontoxic doses of an industrial pesticide emulsifier and subsequently are infected with sublethal doses of mouse-adapted human Influenza B (Lee) virus (FluB). The purpose of this study was to determine whether liver lipid content was altered in the mice, the time course of any changes, and whether lipid changes were consistent with liver pathology. Neonatal mice exposed dermally to the emulsifier, Toximul MP8 (Tox), had significantly elevated levels of hepatic cholesterol, with otherwise normal lipid composition. Subsequent inoculation of the mice with FluB significantly increased mortality rate. The combined Tox + FluB treatment had several significant effects on liver lipids, including a transient increase in phospholipid (PL) content, a reduction in neutral glycerides and persistently high cholesterol levels. Abnormalities in fatty acid profiles included an apparent elevation in medium chain fatty acids and increased ratios of PL arachidonic to docosahexaenoic acids. Histologically, there was no evidence of fat accumulation in the liver; however, hepatic mitochondria had severe structural abnormalities characteristic of RS. These studies demonstrate that chemical-dependent enhancement of viral virulence is associated with significant alterations of hepatic lipids. We believe that these abnormalities are related to mitochondrial structural damage in RS despite the absence of hepatic steatosis.

Animals↗
PubMed1990

Atherosclerosis mouse model induced by a high-cholesterol diet supplemented with beta-aminopropionitrile: effects of various anti-atherosclerotic agents on the biochemical parameters.

A mouse model of atherosclerosis was produced by feeding a 1.5% cholesterol diet with 0.4% beta-aminopropionitrile (BAPN) fumarate, a chemical lathyrogen, for 10 weeks, and the pharmacological sensitivity and specificity of this model were evaluated biochemically with various hypolipidemic drugs and calcium antagonists. Histological findings on this model showed typical angiolathyrism with foam cells in the media of the thoracic aorta. Uniform and marked accumulation of cholesterol, notably esterified cholesterol, in the aorta was observed, although it was much less in mice receiving a high-cholesterol diet or BAPN alone. The reduction in elastin contents in the aorta was a characteristic feature of this model. Clofibrate, cetaben and elastase tended to prevent the increase of cholesterol contents in the aorta, together with their significant hypocholesterolemic effects. Nifedipine, diltiazem and verapamil showed a slight preventive effect on the cholesterol accumulation and on the reduction of elastin content in the aorta without a cholesterol lowering effect in the serum. MgCl2 was more effective than other calcium antagonists and even had a hypocholesterolemic effect. The results indicate that this mouse atherosclerosis model may be usable for primary drug evaluation.

4-Aminobenzoic Acid↗
PubMed1993

Propagation of human papillomavirus type 11 in human xenografts using the severe combined immunodeficiency (SCID) mouse and comparison to the nude mouse model.

We report propagation of human papillomavirus (HPV) type 11 in human xenografts in the severe combined immunodeficiency (SCID) mouse and compare this new animal model for HPV infection to the previously established athymic nude mouse model. HPV-11-infected foreskin fragments grafted under the renal capsule of SCID mice formed large epithelial cysts that had the histologic and immunocytochemical features of HPV infection. This infection was successfully passaged to nude mice. Viral particles that reacted to an antibody directed to HPV-11 virions were identified from samples recovered from the SCID and nude mice. Viral DNA sequence analysis confirmed that the passaged virus was HPV-11. In a comparative experiment of the nude mouse and SCID mouse models, the latter produced HPV-11-infected xenografts that were larger and more often positive for HPV by immunocytochemistry and presence of viral mRNA than those propagated in the former model. Finally, we observed that growth of HPV-11-infected foreskin fragments in the SCID mouse model is not restricted to the kidney as in the nude mouse, but also can occur in the subcutis and the peritoneum.

Animals↗
PubMed1991

Towards a transgenic mouse model of sickle cell disease: hemoglobin SAD.

In order to obtain a transgenic mouse model of sickle cell disease, we have synthesized a novel human beta-globin gene, beta SAD, designed to increase the polymerization of the transgenic human hemoglobin S (Hb S) in vivo. beta SAD (beta S-Antilles-D Punjab) includes the beta 6Val substitution of the beta S chain, as well as two other mutations, Antilles (beta 23Ile) and D Punjab (beta 121Gln) each of which promotes the polymerization of Hb S in human. The beta SAD gene and the human alpha 2-globin gene, each linked to the beta-globin locus control region (LCR) were co-introduced into the mouse germ line. In one of the five transgenic lines obtained, SAD-1, red blood cells contained 19% human Hb SAD (alpha 2 human 1 beta 2SAD) and mouse-human hybrids in addition to mouse hemoglobin. Adult SAD-1 transgenic mice were not anemic but had some abnormal features of erythrocytes and slightly enlarged spleens. Their erythrocytes displayed sickling upon deoxygenation in vitro. SAD-1 neonates were anemic and many did not survive. In order to generate adult mice with a more severe sickle cell syndrome, crosses between the SAD progeny and homozygous for beta-thalassemic mice were performed. Hemoglobin SAD was increased to 26% in beta-thal/SAD-1 mice which exhibited: (i) abnormal erythrocytes with regard to shape and density; (ii) an enlarged spleen and a high reticulocyte count indicating an increased erythropoiesis; (iii) mortality upon hypoxia; (iv) polymerization of hemolysate similar to that obtained in human homozygous sickle cell disease; and (v) anemia and mortality during development.

Anemia, Sickle Cell↗
PubMed1987

Steroid receptors and human endometrial carcinoma: studies in a nude mouse model.

An experimental nude mouse system where human endometrial carcinomas of different histologic grade and steroid receptor characteristics can be grown and maintained under defined hormonal milieu by serial transplantation has been developed. Biologically and clinically important information on the role of steroid receptors in eliciting hormonal responses in these tumors has been obtained using this model. These results form the basis for designing and testing various treatment strategies for endometrial carcinomas of different histologic grade and receptor content.

Animals↗
PubMed1993

A mouse model for varicella-zoster virus latency.

Following primary infection with varicella-zoster virus (VZV), the virus establishes a latent infection in humans. The molecular pathogenesis of VZV latency is not well understood, mainly due to the lack of an adequate animal model. We report here that we have developed a mouse model for VZV infection that involves corneal inoculation of mice. Although infected animals showed no signs of disease, most of the animals could not eliminate the virus early after infection. By PCR, we demonstrated that at 33 days post-infection (p.i.), viral DNA was still present in more than 60% of the animals (14/21). VZV DNA was most frequently detected in the trigeminal ganglia (7/14) followed by the brain stem (10/21), kidneys (4/21), spleen (3/20), liver (2/21) and brain (1/21). By in situ hybridization, a few cells positive for VZV mRNA were detected in the trigeminal ganglia, brain stem, cerebellum and spleen of a small number of the infected animals as late as 33 days p.i. No viral proteins were detected at the site of inoculation or in any other tissue by immunostaining. Our results suggest that VZV spreads in mice by both viraemia and axonal transport and establishes a non-productive (latent) infection.

Animals↗
PubMed2025

Tracking HIV persistence across T cell lineages during early ART-treated HIV-1-infection using a reservoir-marking humanized mouse model.

Human immunodeficiency virus (HIV) infection depletes CD4 T-cells, and long-term persistence of latent virus prevents full clearance of HIV even in the presence of effective antiretroviral therapy (ART), Here we present the HIV-1-induced lineage tracing (HILT) system, a model that irreversibly marks infected cells within a humanized mouse model, which detects rare latently infected cells. Immunodeficient mice transplanted with genetically modified hematopoietic stem cells develop a human immune system, in which CD4 T-cells contain a genetic switch that permanently labels cells infected by HIV-1 expressing cre-recombinase. Through single-cell RNA sequencing of HILT-marked cells during acute infection and post-ART treatment, we identify distinct CD4+ T-cell transcriptional lineages enriched in either active or latent infections. Comparative gene expression analysis highlights common pathways modulated in both states, including EIF2, Sirtuin, and protein ubiquitination. Critical regulators of these pathways, including JUN, BCL2, and MDM2, change to opposite directions in the two states, highlighting gene expression programs that may support HIV persistence across T-cell lineages and states.

Animals↗
PubMed2026

A mouse model of autosomal dominant spastic ataxia and myopathy caused by a mutation in Tuba4a.

Hereditary ataxias are a heterogeneous group of neurodegenerative disorders characterized by impaired balance and coordination, often due to cerebellar dysfunction. Despite advances in identifying genetic causes, animal models remain essential for dissecting underlying mechanisms and testing therapeutic strategies. Here we describe a mouse model of spastic ataxia and myopathy caused by a missense mutation in Tuba4a (n.A626C, p.Gln176Pro). In an ENU mutagenesis screen, a male C57BL/6 J mouse exhibiting muscle wasting and an intention tremor starting at approximately 4 weeks-of-age was identified. The male was bred by in vitro fertilization to BALB/cByJ oocyte donors. Genetic mapping determined dominant inheritance and localized the mutation to Chromosome 1. Genome sequencing revealed single nucleotide polymorphisms (SNPs) in serine threonine kinase 36 (Stk36Y1003N) and alpha-tubulin 4A (Tuba4aQ176P) in the mapping interval. These SNPs were CRISPR-engineered into C57BL/6 J mice, which confirmed the Tuba4aQ176P variant as the causative mutation. Mutant mice are normal at 3 weeks, except for decrement in muscle response following repetitive nerve stimulation. However, by 30 days these mice have overt ataxia, Purkinje neuron degeneration, and extensive skeletal muscle defects, which contribute to a decreased lifespan. Dominant TUBA4A mutations in humans are associated with spastic ataxia type 11 (SPAX11), congenital myopathy type 26 (CMYO26), and frontotemporal dementia/amyotrophic lateral sclerosis type 9 (FTDALS9). Our mice exhibit hallmark features of SPAX11 and CMYO26, but do not show motor neuron degeneration. This specificity makes this model a valuable tool for studying cell-type selective effects of TUBA4A mutations in neurodegeneration and myopathy.

Animals↗
PubMed1994

Herpes simplex virus encephalitis in a mouse model: PCR evidence for CNS latency following acute infection.

We have used a mouse model of herpes simplex encephalitis produced by intranasal inoculation of virus to study the expression of viral immediate early, early and late genes and latency associated transcript (LAT) in trigeminal ganglia and brain at various times after inoculation. A PCR technique was used to detect the viral gene transcripts. All viral genes were expressed between post-inoculation days 1 and 13. On post-inoculation day 42 when the acute infection had subsided only the LAT could be detected, most commonly (70%) in the trigeminal ganglion but also, in 50% of mice, in the brain stem, in 40% in olfactory bulbs and in 20% in cerebrum and cerebellum. These findings suggest that latent infection by HSV-1 may be relatively readily established in the CNS as well as in sensory ganglia. The frequency of establishment of latency appears to be related to the neuroanatomical accessibility of each brain region to the site of entry of the virus.

Animals↗
PubMed1981

Phenytoin-induced teratogenesis: a mouse model.

Malformations associated with the fetal hydantoin syndrome have been reproduced in a mouse model. The occurrence of these defects was correlated with maternal serum concentrations, but not with maternal or fetal genotype or the presence of a seizure disorder.

Animals↗
PubMed1994

Putative anticryptosporidial agents tested with an immunodeficient mouse model.

Lasalocid, sinefungin, and dehydroepiandrosterone were tested for anticryptosporidial activity with an immunodeficient mouse model at doses that have been reported effective when tested with immunosuppressed rodent models. Small but significant reductions in oocyst excretion were only observed under some conditions with lasalocid and dehydroepiandrosterone, but sinefungin had no effect.

Adenosine↗
PubMed1991

Role of influenza B virus in hepatic steatosis and mitochondrial abnormalities in a mouse model of Reye syndrome.

The hepatic steatosis observed in the influenza B virus mouse model of Reye syndrome has been attributed to infectious virus or, alternately, to decreased food intake in the virus-treated mice or impurities in the virus preparation. To resolve this issue, 4- to 6-wk-old male Balb C mice were given, by intravenous injection, 12,800 hemagglutination units of influenza B Lee/40 virus in phosphate buffered saline/1% bovine serum albumin using virus prepared by ultra-centrifugation from infected allantoic fluid, by sucrose density-gradient purification of virus prepared by ultracentrifugation from infected allantoic fluid or by irradiation of virus prepared by ultracentrifugation from infected allantoic fluid to inactivate virus. The infectivity titer of virus prepared by ultracentrifugation from infected allantoic fluid was much higher than that of sucrose density-gradient purified virus prepared from infected allantoic fluid: 50% egg infectious dose for virus prepared by ultracentrifugation from infected allantoic fluid was 3.9 x 10(4)/hemagglutination unit vs. 8.7 50% egg infectious dose/hemagglutination unit for sucrose density-gradient purified virus prepared from infected allantoic fluid. Control mice received phosphate-buffered saline/1% bovine serum albumin or uninfected allantoic fluid diluted in phosphate-buffered saline/1% bovine serum albumin. Mice were fasted to eliminate dietary variation, and livers were obtained 36 hr after virus administration. Of the above treatments, only virus prepared by ultracentrifugation from infected allantoic fluid caused clinical illness and increased hepatic triglycerides (p less than 0.02) compared with controls. Hepatic triglycerides in virus prepared by ultracentrifugation from infected allantoic fluid correlated with histopathological vacuolization scores (r = 0.5773; p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Suckling mouse model for detection of heat-stable Escherichia coli enterotoxin: characteristics of the model.

Although the suckling mouse assay is widely used for the detection of heat-stable Escherichia coli enterotoxin (ST), few data have been published concerning the reproducibility, optimal growth, and test conditions of this assay. Four strains of toxigenic E. coli known to elaborate both heat-labile enterotoxin and ST or ST alone were used to study these parameters. ST activity after heat treatment and the effect of purified choleragen were also examined. ST production was optimal in Casamino Acids-yeast extract media, but both Trypticase soy and brain heart infusion broths resulted in several false negative reactions. Growing cultures in roller tubes was the most reliable method of ST production. Shaking-flask cultures and stationary-grown cultures resulted in suboptimal ST production in several strains. Optimal mouse incubation time was 3 h, and fluid secretion did not rise thereafter. Adequate toxin production occurred after 16 to 24 h of incubation. The coefficient of variation of various toxins tested on many occasions varied between 10.5 and 15.7%. Toxin activity was stable for 6 months when frozen at - 20 C. There was no decrease in ST activity when heated at 65 C for 15 min, but a small decrease was observed in two of four strains after heating at 100 C for 30 min. Choleragen, tested at various doses and at multiple times, gave uniformly negative results. These studies indicate that when done under the proper conditions, the suckling mouse assay is a simple, rapid, and reproducible assay for E. coli ST.

Animals↗
PubMed1993

Opsin synthesis in the C57BL/6-mivit/mivit mouse model of retinal degeneration.

The capacity of photoreceptor cells to synthesize opsin was evaluated in a newly-described mouse model of retinal degeneration, the C57BL/6-mivit/mivit. The mivit/mivit mouse loses photoreceptor cells at a rate of about one row per month beginning at 8 weeks, ROS are severely disrupted at 4 months, RPE is unevenly pigmented. Retinas of affected and control mice ages 4, 6, 8, 12, 16, 20, 24, 28, 32 and 52 weeks were incubated for 2 hours in medium containing [3H] leucine. Homogenates of retina samples were subjected to SDS-PAGE using disc gels. The gels were sliced and counted by scintillation. The incorporation of [3H] leucine into opsin was compared with its incorporation into other retinal proteins. During the early time points studied, mivit/mivit retinas incorporated proportionately similar amounts of [3H] leucine into opsin versus other retinal proteins as did controls. At 12 weeks, the percentage was about 80% and it continued to decline over the succeeding weeks studied. By 1 year, the proportion of leucine incorporated into opsin versus other proteins was only about 23% the amount incorporated in controls. The results of the present study suggest that the mivit/mivit photoreceptor cells are able to synthesize opsin and the gradual decline in synthetic ability follows the gradual loss of cells and is not correlated with the disruption of ROS.

Aging↗
PubMed1986

Genetic basis for a mouse model of Down syndrome.

The Trisomy 16 (Ts16) mouse has been proposed as a model for Down Syndrome (DS) in humans, based on genetic homology between mouse chromosome 16 (MMU 16) and human chromosome 21 (HSA 21). Translocations of HSA 21 resulting in trisomy for only a portion of the genetic information contained on this chromosome can result in a DS phenotype. Thus, these translocations help to define a "DS region" of the chromosome. A number of genes from this DS region of HSA 21 have been mapped to MMU 16. Techniques for localizing genes on chromosomes have been used to identify the portion of MMU 16 which corresponds to the DS region of HSA 21. This region appears to be highly conserved between mouse and human, providing further support for a mouse model of DS.

Animals↗
PubMed1987

Comparison of detection procedures for Chlamydia trachomatis, including enzyme immunoassays, in a mouse model of genital infection.

Two chlamydial enzyme immunoassays, Chlamydiazyme and IDEIA, were evaluated in a mouse model of chlamydial genital-tract infection. The Chlamydiazyme assay and the IDEIA were assessed on specimens from 10 and 11 mice, respectively. The animals were infected with Chlamydia trachomatis, strain SA2f, and the results obtained by these methods on vaginal specimens taken on 4 or 5 occasions during 41-42 days were compared with those obtained in cell culture and to a less extent by the MicroTrak direct immunofluorescence test. In comparison with culture, the Chlamydiazyme assay had a sensitivity of 62% and a specificity of 92%; IDEIA had a sensitivity of 76% and a specificity of 94%. These assays sometimes did not detect chlamydiae in specimens taken immediately before specimens which proved positive by culture and the immunoassays were less sensitive if swabs were taken after those for culture. The IDEIA also failed to detect chlamydiae in the late stage of the murine infection when chlamydial elementary bodies were seen by immunofluorescence. The implications of the observations for investigations in the human field as well as for further studies in the mouse are discussed.

Animals↗