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At least 19 recordsLinked to original sources

[Susceptibility of the macrophages of inbred strain mice to Chlamydia psittaci].

Chlamydia psittaci was injected in the peritoneal cavity of different strains of inbred mice. Not all of them develop a clinical disease; some, such as C 3 H, are very susceptible and died within 6 days. C 57 BL, however, are resistant even to a very high dose. We still do not know the exact mechanism of the natural resistance. This is the reason why we are trying to analyse the role of the macrophage. This cell is particularly important in C. psittaci infection, because it harbours the obligate intracellular organisms which multiply inside the cytoplasm. Peritoneal macrophages of three different strains of mice (C 3 H, AKR and C 57 BL) were cultured following Fauve's technique [4]. 48 h after, the macrophages were inoculated with a suspension of C. psittaci. Hela 229 were used as control. 48, 78 and 92 h after inoculation, amount of inclusion in each category of macrophages and Hela cells was determined. C 57 BL macrophages cultured from mice resistant to Chlamydia psittaci allowed the in vitro multiplication of the same bacteria: 72 h after inoculation, 100% of the macrophages were infected and a large inclusion could be seen. C 3 H macrophages cultured from mice very susceptible to Chlamydia psittaci seemed less susceptible in vitro than the C 57 BL macrophages; 72 h after inoculation, 50% only of the infected macrophages showed intracytoplasmic inclusion: AKR macrophages were also susceptible, although AKR mice recover from C. psittaci infection. In conclusion, the difference of susceptibility, as displayed by several strains of inbred mice infected by C. psittaci, cannot be explained by the difference of susceptibility of their macrophages.

Animals↗

DNA excision-repair ability of embryonic fibroblasts measured by UDS and thymine dimer excorporation in four inbred mice strains.

Differences in the excision-repair capability of embryonic fibroblasts of four inbred strains of mice following various degrees of UV irradiation were assessed. Two methods of determination were used: (1) the incorporation of 3H-thymidine during unscheduled DNA synthesis (UDS) as measured by an autoradiographic technique; (2) the rate of excision of thymine dimers (TT) in the acid-insoluble fraction of the cellular DNA as determined by a dimerspecific radioimmuno-assay. Based on UDS, the repair rates of the four strains could be ranked in decreasing order as follows: DBA/2 (DB); C57BL/6J (B6); AKR/N (AK); CBA/J (CB). The calculated rate for DBA/2 (DB) is approximately twice that of CBA/J (CB). The determination of the TT excision rate indicates that 72 h after irradiation a maximum of 50% of the original UV-induced dimers in the DB strain could be repaired. In the three remaining strains the relatively reduced repair rates of 15% - 40% did not differ significantly.

Animals↗

Toxic effect of lead on fertility of inbred strain mice.

Males of inbred strains were orally given lead acetate water solution during 150 days. Changes were found in the structure of the seminiferous tubules and in spermatozoa. The pathological changes in Leydig cells brought about a decline in levels of androgens.

Androgens↗

Susceptibility to Mycobacterium tuberculosis: lessons from inbred strains of mice.

Inbred strains of mice exhibit varied patterns of susceptibility following infection with virulent Mycobacterium tuberculosis. Susceptible mice have progressive fulminate disease resulting in their premature death; in contrast, resistant mice are able to control bacterial replication, limit lung injury and survive longer. The use of these mouse strains in experimental infection has allowed the identification of immunological correlates of protective versus unsuccessful host responses to tuberculosis, and the identification of susceptibility loci by combining classical and molecular genetics. These immunological and genetic features that distinguish susceptible and resistant inbred mouse strains may allow us to better understand susceptibility to tuberculous disease in people. A possible benefit would be the delineation of markers of protective immunity for use in vaccine development. This is a review of recent insights into the genetics and immunology of resistance and susceptibility to virulent M. tuberculosis using genetically intact mice.

Animals↗

Role of complement components in the susceptibility to Plasmodium berghei infection among inbred strains of mice.

Inbred strains of mice, sensitive and resistant to Plasmodium berghei infections, including a complement deficient strain were infected with P. berghei. Daily levels of parasitaemia were determined and serum levels of complement components (C3 and C5) measured by standard haemolytic assay. Serum levels of C3 and C5 were depressed in all strains of mice infected with P. berghei. There was no difference in the infectivity and course of P. berghei infection in the co-isogenic C5 deficient and non-deficient strains. The significance of these observations is discussed.

Agglutination Tests↗

Comparative teratogenicity of phenytoin among several inbred strains of mice.

Inbred strains of mice differ in their response to the embryopathic effects of phenytoin (PHT). A/J animals, the most susceptible strain, were mated to C57BL/6J mice, the most resistant strain. The susceptibility of the F1 hybrid offspring was determined by the susceptibility of the mother. B6AF1 animals were as resistant as C57BL/6J parental mice, and AB6F1 hybrids were as susceptible as A/J mice. This was especially evident when orofacial anomalies were tallied. (B6A)F2 hybrid offspring were as resistant as their C57BL/6J grandparents.

Abnormalities, Drug-Induced↗

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.

Animals↗

A major gene affecting age-related hearing loss is common to at least ten inbred strains of mice.

Inbred strains of mice offer promising models for understanding the genetic basis of human presbycusis or age-related hearing loss (AHL). We previously mapped a major gene affecting AHL in C57BL/6J mice. Here, we show that the same Chromosome 10 gene (Ahl) is a major contributor to AHL in nine other inbred mouse strains-129P1/ReJ, A/J, BALB/cByJ, BUB/BnJ, C57BR/cdJ, DBA/2J, NOD/LtJ, SKH2/J, and STOCK760. F1 hybrids between each of these inbred strains and the normal-hearing inbred strain CAST/Ei retain good hearing, indicating that inheritance of AHL is recessive. To follow segregation of hearing loss, F1 hybrids were backcrossed to the parental strains with AHL. Auditory-evoked brain-stem response thresholds were used to assess hearing in more than 1500 N2 mice and analyzed as quantitative traits for linkage associations with Chromosome 10 markers. Highly significant linkage was found in all nine strain backcrosses, with the highest probability (LOD > 70) near the marker D10Mit112. This map position for Ahl is near the waltzer mutation (v) and the modifier of deaf waddler locus (mdfw), suggesting the possibility of allelism. Results from an intercross of C57BL/6J and NOD/LtJ mice indicate that the 6- to 10-month difference in AHL onset between these two strains is not due to allelic heterogeneity of the Ahl gene.

Aging↗

Mechanisms in in vivo release of lymphokines. III. Separation of gamma-interferon (IFN gamma) from cytotoxicity in inbred strains of mice.

Inbred strains of mice sensitized with BCG and challenged with old tuberculin (OT) vary in their capacity to release IFN gamma and MIF into circulation. Experiments were performed to correlate the presence of IFN gamma with that of the cytotoxic effect in an attempt to learn whether these two activities in the sera may be separated. Sera from eight inbred strains were obtained at times after challenge and assayed for IFN and for cytotoxic activity. A correlation did not exist between the titers of IFN gamma and the levels of cytotoxicity, i.e. sera from RF/J mice without detectable titers of IFN gamma had cytotoxic activity, while sera from C57BL/KsJ mice that had titers of IFN gamma were not cytotoxic. Regulation of IFN gamma titers could be achieved by administration of complete Freund's adjuvant to BCG sensitized mice. However, similar differences were not detected in cytotoxic activity. Therefore, IFN gamma may be released, or the activity of IFN gamma may be expressed in the circulation, in the absence of cytotoxicity.

Adjuvants, Immunologic↗

Age-related changes in the motricity of the inbred mice strains 129/sv and C57BL/6j.

The development of motor skills was studied at different stages in the life of the mouse, focusing on three key aspects of motor development: early rhythmic motor activities prior to the acquisition of quadruped locomotion, motor skills in young adults, and the effect of aging on motor skills. The age-related development pattern was analysed and compared in two strains of major importance for genomic studies (C57Bl6/j and 129/sv). Early rhythmic air-stepping activities by l-dopa injected mice showed similar overall development in both strains; differences were observed with greater beating frequency and less inter-limb coordination in 129/sv, suggesting that 129/sv had a different maturation process. Performance on the rotarod by young adult C57Bl6/j gradually improved between 1 and 3 months, but then declined with age; performance on the treadmill also declined with an age-related increase in fatigability. Overall performance by 129/sv mice was lower than C57Bl6/j, and the age-related pattern of change was different, with 129/sv having relatively stable performance over time. Inter-strain differences and their possible causes, in particular the role of dopaminergic pathways, are discussed together with repercussions affecting mutant phenotyping procedures.

Aging↗

[Renewal of noradrenaline in different zones of the central nervous system of inbred mice strains and their recombinants].

A good correlation exists between the learning capacity and norepinephrine metabolism in the neocortex of C57 and Balb inbred Mice strains, as well as their F1 hybrids and seven recombinant inbred strains derived from their cross. The animals with a better learning performance are characterised by low levels of norepinephrine, as well as a slow metabolic rate of this neurotransmitter in the cortex. Such a correlation has not been found to exist in the other cerebral regions studied.

Animals↗

Alcohol-induced locomotor activation in C57BL/6J, A/J, and AXB/BXA recombinant inbred mice: strain distribution patterns and quantitative trait loci analysis.

RATIONALE: Quantitative trait loci (QTLs) for initial sensitivity to alcohol have been identified in a number of mouse strains (e.g. BXD); however, confirmation is required. OBJECTIVES: The present paper aimed to characterize the C57BL/6J, A/J, and AXB/BXA recombinant inbred (RI) strains of mice for basal and ethanol-induced locomotor activation as measured in an open field and to provide provisional location of QTLs for these phenotypes. METHODS: A/J and C57BL/6J mice were habituated to handling and then randomly assigned to receive one of four alcohol doses (0, 0.5, 1.0, 2.0 g/kg). Subsequently, all available strains of the AXB/BXA RI were tested with the 2 g/kg dose of ethanol or vehicle control. RESULTS: Simple regression and interval mapping were used initially to identify significant gene markers associated with ethanol-induced activation (calculated as total activity on alcohol day-total activity on saline day). Subsequently, composite interval mapping (CIM) was used to increase the accuracy in mapping individual loci. Genetic markers on chromosomes 2, 3, 8, 13, 16, 18 and 19 were associated with ethanol-induced activation. CONCLUSIONS: Three significant markers identified through CIM accounted for 86% of the genetic variance in the ethanol-induced activation. QTLs on chromosome 16 (45.6 cM) and 19 (24 cM) previously associated with alcohol consumption in the AXB/BXA RI mice were found to overlap with QTLs for ethanol-induced activation identified in the present study.

Animals↗

Systematic, standardized and comprehensive neurological phenotyping of inbred mice strains in the German Mouse Clinic.

Neurological and psychiatric disorders are among the most common and most serious health problems in developed countries. Transgenic mouse models mimicking human neurological diseases have provided new insights into development and function of the nervous system. One of the prominent goals of the German National Genome Research Network is the understanding of the in vivo function of single genes and the pathophysiological and clinical consequences of respective mutations. The German Mouse Clinic (GMC) offers a high-throughput primary screen of genetically modified mouse models as well as an in-depth analysis in secondary and tertiary screens covering various fields of mouse physiology. Here we describe the phenotyping methods of the Neurological Screen in the GMC, exemplified in the four inbred mouse lines C57BL/6J, C3HeB/FeJ, BALB/cByJ, and 129S2/SvPas. For our primary screen, we generated "standard operating procedures" that were validated between different laboratories. The phenotyping of inbred strains already showed significant differences in various parameters, thus being a prerequisite for the examination of mutant mouse lines.

Analysis of Variance↗

Differences in resistance to Trypanosoma musculi infection among strains of inbred mice.

Inbred strains of mice were inoculated with Trypanosoma musculi, and the course of the ensuing parasitemia was followed. The mouse strains fell into three groups: those displaying high and moderate (fivefold less) parasitemia and C57BL/6 (B/6) mice which had exceptionally low infections. To gain insight concerning the mechanisms responsible for interstrain variations in infections, several types of experiments were performed. Comparison of the ability of spleen cells from the various strains to provide the growth-promoting substances required by T. musculi for growth in culture revealed that B/6 cells were deficient; this suggested one mechanism for regulating parasite infections. Exposure of C3H (high parasitemia) and B/6 mice to graded levels of ionizing radiation revealed that B/6 mice have much greater innate resistance to infection than do C3H mice. The effects of treating mice with silica dust or mercaptoethanol indicated that relative resistance to infection is not primarily associated with macrophage activity or limited growth-promoting substances. We conclude that variations in immune responsiveness to parasite antigens (probably not associated with the H-2 complex), possibly in concert with variations in a non-immunological mechanism, account for interstrain variation in resistance to T. musculi infections.

Animals↗

Genetic analysis of rapid tolerance to ethanol's incoordinating effects in mice: inbred strains and artificial selection.

Ethanol tolerance, a decrease in drug responsiveness with repeated administrations, is an important diagnostic criterion for alcoholism. Rapid tolerance develops within 8-24 hours of an initial ethanol exposure and shares many similarities with chronic tolerance. The genetic contribution to rapid tolerance to ethanol-induced ataxia was estimated using a panel of inbred strains of mice. Strains differed significantly in the degree of rapid tolerance development, which had a broad-sense heritability estimate of 0.11. Artificial selection was carried out to develop lines of mice that would show High (HRT) and Low (LRT) levels of Rapid Tolerance. Starting with HS/Npt mice, derived from a systematic cross of eight inbred strains, a significant response to selection was seen in replicate 1 by the third selection generation. No difference was found in replicate 2. Heritability estimates after the fourth generation were 0.25 for HRT-1 mice and 0.06 for LRT-1 mice. HRT-1 and LRT-1 mice also differed significantly in chronic tolerance development to four doses of ethanol. These studies provide evidence for a genetic contribution to rapid tolerance and support a genetic link between rapid and chronic tolerance to ethanol's ataxic effects.

Animals↗

Genetic complementation of defects in vaccine-induced immunity against Schistosoma mansoni in P- and A-strain inbred mice.

Inbred P- and A-strain mice are deficient in their capacity to develop resistance to challenge infection in response to vaccination with irradiated cercariae of Schistosoma mansoni and are also defective in their cell-mediated response as assessed by the activity of antigen-elicited macrophages in killing schistosome larvae in vitro. In contrast, vaccinated (P x A)F1 mice displayed high levels of both immunity to challenge and macrophage larvicidal activity, indicating that the P- and A-strain defects in the vaccine-induced response are controlled by distinct genetic loci.

Animals↗