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PubMed1989

Mouse strains with typical mammalian levels of complement activity.

Common laboratory mouse strains have very low complement levels relative to humans, rats, guinea pigs, rabbits and other mammals, which limits the value of the mouse as an experimental model. We therefore tested serum complement levels of 43 mouse strains and 11 rat strains, for the purpose of selecting a convenient laboratory animal having high complement levels. Total complement activity was determined with both erythrocytes and human tumor cells as targets. Eight mouse strains were identified that have complement levels comparable to those of other mammals. These mouse sera lyse tumor cell targets as well as sera from humans, rats or guinea pigs, although they are somewhat less active than rabbit sera. They are relatively inefficient in lysing erythrocyte targets, yet are as active as rabbit serum in this assay. Target cell lysis was demonstrated to be via the classical pathway of complement activation. Of the eight 'high complement' mouse strains, four were recently derived from wild mice, and one, SF/CamEi, was derived from wild mice in 1951. The three other strains, BUB/BnJ, DA/HuSn and RIIIS/J, were developed more than 40 years ago, but apparently were not tested previously for complement activity. Using the BUB mouse as a representative of the 'high complement' mice, we assayed levels of the nine complement components, in an attempt to identify the cause of high complement activity. No difference in levels of C1, C2, C4, C8 or C9 was detected between BUB and BDF1 mice. C2 activity was very low in both strains. C3, C5, C6 and C7 activities were higher in BUB mice than in BDF1 mice, indicating that variation in these complement components is responsible for the difference in total complement activity. The genes determining the 'high complement' phenotype appeared to be semi-dominant in F1 hybrids. The 'high-complement' mouse strains, and recombinant strains derived from them, will be useful in a wide range of biomedical research.

Animals↗
PubMed1993

Genetic selection for crescent formation yields mouse strain with rapidly progressive glomerulonephritis and small vessel vasculitis.

We have established a recombinant inbred strain of mouse named spontaneous crescentic glomerulonephritis-forming mouse/Kinjoh or SCG/Kj. Mice of this strain spontaneously develop rapidly progressive glomerulonephritis. This strain of mice was derived from (BXSB/Mp x MRL/Mp-lpr/lpr)F1 hybrid mice by brother x sister mating coupled with repeated histopathologic selection for breeding of mice whose parents had the highest frequency of crescent formation in the kidneys. In this strain of mice, nephritis appears earlier and is more rapidly progressive than in any other murine model of systemic lupus erythematosus. Histopathologically, the characteristic renal lesions in the mice of this strain express a most dramatic form of crescentic glomerulonephritis. The lesions in the kidneys show only slight fine granular immune deposits along the glomerular basement membrane associated with remarkable extraglomerular proliferation and hemorrhage in Bowman's space. Although selection was not based on vasculitis, mice of this strain also exhibit a high incidence of necrotizing vasculitis. These vascular lesions involve primarily small arteries and arterioles and many organs and tissues but spare the kidneys. Thus this form of vasculitis has been found to be correlated with the crescentic form of glomerulonephritis but not with lymphoid hyperplasia of the spleen. We conclude that, in this strain of mouse, the rapidly progressive glomerulonephritis is genetically restricted and that this genetic restriction is firmly linked to that responsible for the vasculitis.

Animals↗
PubMed2004

Polymorphisms in the taste receptor gene (Tas1r3) region are associated with saccharin preference in 30 mouse strains.

The results of recent studies suggest that the mouse Sac (saccharin preference) locus is identical to the Tas1r3 (taste receptor) gene. The goal of this study was to identify Tas1r3 sequence variants associated with saccharin preference in a large number of inbred mouse strains. Initially, we sequenced approximately 6.7 kb of the Tas1r3 gene and its flanking regions from six inbred mouse strains with high and low saccharin preference, including the strains in which the Sac alleles were described originally (C57BL/6J, Sac(b); DBA/2J, Sac(d)). Of the 89 sequence variants detected among these six strains, eight polymorphic sites were significantly associated with preferences for 1.6 mm saccharin. Next, each of these eight variant sites were genotyped in 24 additional mouse strains. Analysis of the genotype-phenotype associations in all 30 strains showed the strongest association with saccharin preference at three sites: nucleotide (nt) -791 (3 bp insertion/deletion), nt +135 (Ser45Ser), and nt +179 (Ile60Thr). We measured Tas1r3 gene expression, transcript size, and T1R3 immunoreactivity in the taste tissue of two inbred mouse strains with different Tas1r3 haplotypes and saccharin preferences. The results of these experiments suggest that the polymorphisms associated with saccharin preference do not act by blocking gene expression, changing alternative splicing, or interfering with protein translation in taste tissue. The amino acid substitution (Ile60Thr) may influence the ability of the protein to form dimers or bind sweeteners. Here, we present data for future studies directed to experimentally confirm the function of these polymorphisms and highlight some of the difficulties of identifying specific DNA sequence variants that underlie quantitative trait loci.

Animals↗
PubMed1982

Ethanol and simulated high altitude. A study of three mouse strains.

The effect of short-term exposure of three mouse-strains to simulated high altitude (SHA) of approximately 6,000 m was studied. Subjecting C57BL/6J, DBA/2J or albino mouse strains to SHA for 39 days, occurring on alternating days, increased liver weight in the albino mouse compared to controls. The C57BL strain showed increased growth during SHA compared to other mouse strains. Morbidity score was greater in the albino mouse than in DBA mouse with no death occurring in C57BL mice exposed to SHA. Hepatic alcohol dehydrogenase was induced and mitochondrial aldehyde dehydrogenase was inhibited from corresponding controls subsequent SHA exposure by the C57BL and by the DBA mouse strain, respectively. The onset of ethanol-mediated narcosis was decreased from controls subsequent 21 days of SHA exposure by the DBA and by the albino mouse strain. The central depressant action of ethanol, as measured by the duration of ethanol-narcosis, was decreased in the C57BL mice exposed to SHA for 8, 21, or 35 days compared to controls. No apparent changes occurred in duration of ethanol-narcosis in the other mouse strains. The results suggest strain-difference in response to hypobaric conditions.

Acetaldehyde↗
PubMed1990

A congenic line of the BALB/c mouse strain with the endogenous mouse mammary tumor virus proviral gene Mtv-3: tissue-specific expression and correlation with resistance to mouse mammary tumor virus infection and tumorigenesis.

Mouse mammary tumor virus (MMTV) expression and MMTV-induced tumorigenesis were studied in a congenic line of the BALB/cHeA strain, termed BALB/c-Mtv-3+, that carries the Mtv-3 proviral gene. BALB/c-Mtv-3+ mice were free of milk-transmitted MMTV and did not spontaneously develop mammary tumors. A specific Mtv-3 expression was observed in the mammary gland and spleen, but not in other lymphoid tissues, such as thymus and bone marrow. This expression was hormone dependent, as shown by the increase of MMTV mRNA during pregnancy. At the protein level, large amounts of p28, but only traces of gp52, the main MMTV core and envelope antigens, respectively, were observed, in agreement with the already described "partial" expression of the Mtv-3 gene products. The presence of the 24S (3.8 kilobases) mRNA encoding the MMTV env antigens in the spleen and the low gp52 reactivity in lactating mammary glands showed that this noncoordinate expression was probably due to a defect in translation or posttranslational processing of env proteins. The susceptibility of BALB/c-Mtv-3+ to experimental MMTV infection was studied. The presence of Mtv-3 conferred to BALB/c mice resistance to MMTV infection, as shown by measuring viral antigens released in the milk of infected mice and by recording the incidence of early mammary tumors. The presence of a nontumorigenic endogenous MMTV gene was therefore protective against exogenous MMTV infection.

Animals↗
PubMed1991

A murine model for type III tyrosinemia: lack of immunologically detectable 4-hydroxyphenylpyruvic acid dioxygenase enzyme protein in a novel mouse strain with hypertyrosinemia.

We have characterized a new mutant strain of mouse that has hypertyrosinemia. The blood tyrosine level was persistently high, and increased amounts of 4-hydroxyphenylpyruvic acid and its derivatives were excreted into the urine. Succinylacetone was not detected in urine samples from these mice. All the animals were apparently healthy, and there was no evidence of hepatorenal dysfunction. The hypertyrosinemia was transmitted through an autosomal recessive inheritance. Analyses of hepatic enzymes related to tyrosine metabolism revealed that 4-hydroxyphenylpyruvic acid dioxygenase activity was virtually absent, while fumarylacetoacetase and tyrosine aminotransferases (cytosolic and mitochondrial forms) were normal in these mutant mice. Immunoblot analysis of 4-hydroxyphenylpyruvic acid dioxygenase protein in the liver indicated that the subunit protein of the enzyme was absent. It would appear that hypertyrosinemia in this mutant strain was caused by a genetic defect in 4-hydroxyphenylpyruvic acid dioxygenase. These features are similar to type III tyrosinemia in humans. Analysis of this mutant strain of mouse is expected to provide valuable information on the pathogenesis of human type III tyrosinemia and can also serve as a useful system for studies on tyrosine metabolism.

4-Hydroxyphenylpyruvate Dioxygenase↗
PubMed1986

Rates of micronuclei induction in different mouse strains.

It has previously been shown that the inbred mouse strain MS/Ae was more sensitive in the micronucleus test to several mutagenic agents than outbred mice. To elucidate the possible influence of inbreeding, several inbred strains including MS/Ae, AKR, BALB/c, C57 BR were compared to the two OF1 and NMRI outbred strains. The 3 mutagenic agents MNNG, MMC and MMS all induced a significantly higher number of micronuclei in the MS/Ae strain than in any of the other mouse strains. AKR was especially resistant to the alkylating agents MMS and MNNG. Hence, except for the MS/Ae mouse strain, no inbred strain showed a systematically higher sensitivity than the outbred strains for all of the 3 mutagenic agents used.

Animals↗
PubMed2004

A behavioural characterisation of the FVB/N mouse strain.

The use of transgenic models in scientific research has made an enormous contribution to our understanding of the causes and symptoms of many diseases, including neurodegenerative conditions such as Alzheimer's Disease (AD) and Parkinson's Disease (PD). In the creation of transgenic models of neurodegenerative disease, effects of the background strain of the animal on the resulting genotype must be taken into consideration. This is particularly true for behavioural studies in which the background strain of the mouse may mask the phenotype of the genetic manipulation. Here, the behaviour of two mouse strains used in transgenic models, FVB/N and C57BL6/J, were compared. Studies of circadian wheel activity, cognition and aggression revealed considerable phenotypic differences between strains. These data also indicate that the FVB/N strain is not appropriate as a background strain in the behavioural assessment of transgenic mouse models.

Aggression↗
PubMed2004

Susceptibility of various mouse strains to systemically- or aerosol-initiated tularemia by virulent type A Francisella tularensis before and after immunization with the attenuated live vaccine strain of the pathogen.

The following study determined whether commonly available mouse strains could be used to reveal vaccines capable of protecting against aerosol exposure to virulent type A strains of Francisella tularensis. The attenuated live vaccine strain (LVS) of the pathogen, F. tularensis LVS, was used as the model vaccine for these studies. The results showed that most mouse strains survived intradermal immunization with 10(5)cfu of LVS, except for A/J mice the majority of which died following exposure to 10(4)cfu (colony forming units). Most LVS-immunized mouse strains survived subsequent i.d. challenge with >50 LD(50) of a virulent type A strain of the pathogen. However, all mouse strains tested remained susceptible to lethal infection by a low dose ( approximately 20 cfu) aerosol challenge with virulent F. tularensis even after vaccination with LVS, though immunized C3H/HeN mice appeared to be slightly more resistant than the rest to such an assault.

Animals↗
PubMed1998

Experimental infection of inbred mouse strains with Spironucleus muris.

Four inbred mouse strains: BALB/c ByJ, 129/J, C3H/HeJ, and DBA/lJ, differing in major histocompatibility type, were orally inoculated with 2 x 10(5) infectious cysts of Spironucleus muris. Fecal samples were collected for fecal cyst output prior to infection, and on days 2, 6, 7, 8, 9, 11, 13, 15, and 17 after infection. Following necropsy, formalin-fixed intestinal sections were examined for the presence of trophozoites. On post-inoculation days 6 and 8, mice of the 129/J strain shed significantly (p<0.05) fewer cysts than other strains. This pilot study suggests that major histocompatibility haplotype may influence susceptibility of inbred mouse strains to S. muris.

Animals↗
PubMed1992

V beta 17 T-cell deletion by endogenous mammary tumor virus in wild-type-derived mouse strain.

The wild-type-derived mouse strain PWK possesses a beta-chain variable region V beta 17a2 allele, which is expressed on mature T cells as part of the T-cell receptor of most mice expressing I-E, whereas V beta 17 T cells are deleted in all I-E+ laboratory mice bearing a V beta 17a1 allele. However, (PWK x CBA/J)F1 progeny and the wild-type-derived mouse strain MAI, which possesses the V beta 17a2 allele, display deletion of V beta 17 T cells. Analysis of (PWK x CBA/J) x PWK and of (PWK x MAI) x PWK backcrosses demonstrates that endogenous mouse mammary tumor virus MTV-6 from CBA/J and a MTV from strain MAI control the clonal deletion of V beta 17a2 as well as V beta 3 T cells. Furthermore, among I-E- progeny of a (MAI x C57BL/6) x C57BL/6 backcross, we observed that mice inheriting MTV of MAI have a reduced level of V beta 17 T cells, suggesting that the clonal deletion of V beta 17a2 T cells can be mediated in the absence of the I-E molecule. The 3' long terminal repeat of MTV MAI was cloned and translation of the open reading frame was compared to those of MTV known to encode superantigens. Comparisons indicate that MTV MAI has significantly diverged from the other MTVs. However, MTV MAI and MTV-6 share a stretch of 11 identical amino acids at the C terminus, which is divergent in MTV reacting with other V beta s. This suggests that this region is involved in determining the specificity toward V beta s and has been selectively conserved through evolution of the Mus species.

Alleles↗
PubMed1977

Transmission of mammary tumor virus in mouse strain DD: further support for the uniqueness of strain GR.

Outcrosses between high tumor mouse strain DD and low-incidence strains BALB/c and C57BL to produce reciprocal F1 susceptible offspring of both types resulted in high incidences of mammary tumors in (DD female X BALB/c male)F1 and (DD female X C57BL male)F1 females but not in the reciprocal hybrids with DD as the male parent. The finding that transmission of murine mammary tumor virus (MuMTV) in DD was through the milk, as most often observed in mouse strains, further supported the uniqueness of strain GR in which MuMTV is transmitted by either parent.

Animals↗
PubMed1998

Activation of natural killer cells in arthritis-susceptible but not arthritis-resistant mouse strains following Borrelia burgdorferi infection.

Infection of susceptible mouse strains with Borrelia burgdorferi, the agent of Lyme disease, results in the development of arthritis. Components of the innate immune system may be important mediators of this pathology. To investigate the potential role of NK cells in development of experimental Lyme arthritis, we examined their activation in vivo in both resistant and susceptible mouse strains. Following inoculation of B. burgdorferi into the footpad, lymph node NK cells from susceptible C3H/HeJ (C3H) mice produced more gamma interferon than NK cells from resistant DBA/2J mice. Lymph node cells from susceptible C3H and AKR mice also had increased ability to lyse YAC-1 target cells 2 days following infection. Antibody depletion of NK cells from susceptible mice, however, did not alter the development of arthritis following B. burgdorferi challenge. In addition, NK cell depletion had little effect on spirochete burden. Thus, there is a marked activation of NK cells in susceptible mouse strains following infection. Although NK cells are not absolutely required for arthritis, events occurring prior to NK cell activation might be important in mediating pathology in experimental Lyme disease.

Animals↗
PubMed1996

Experimental melioidosis in inbred mouse strains.

Experimental infection was induced in three inbred mouse strains (BALB/c, BDF1 hybrid and C57BL) by i. p. inoculation with Pseudomonas pseudomallei. The bacterial load in the viscera and the host response induced in different compartments (blood, peritoneal cavity and organs) were determined. Blood cell parameters and peritoneal exudative cell populations were evaluated during the infection with the aid of an automated haematology analyser Technicon H-1. It was found that all mouse strains produced a similar intraperitoneal inflammatory response with predominance of granulocytes at the early stage of infection and subsequent increase of macrophages especially in BDF1 hybrid and BALB/c mice. The highest bacterial count found in the liver and spleen of C57BL was associated with corresponding tissue damage (purulent pneumonia, abscesses in liver, karyorrhexis of hepatocytes and meningoencephalitis). The degree of bacterial load and histological changes found in BALB/c and BDF1 hybrid mice were lower than in C57BL mice. The results show that the variations in the infection magnitude among inbred mouse strains are host-dependent.

Animals↗
PubMed1987

Identification of I-E alpha genes in H-2 recombinant mouse strains by F1 complementation.

Nine recombinant H-2 mouse strains with crossovers in the I region between I-E-negative haplotypes f,q and I-E-positive haplotypes p,k were examined for I-E expression by microcytotoxicity dye exclusion assay. These recombinants were found to be negative for I-E expression. There are two possible genotypes in these recombinant mouse strains that could result in lack of I-E expression. Recombinants with crossovers between the E alpha gene and the S region would have both nonexpressed I-E alpha and beta genes (E beta fE alpha f, E beta qE alpha q) and recombinants with crossovers between the E beta and E alpha genes would have a nonexpressed E beta gene (E beta f or E alpha q) and a functional E alpha gene (E alpha k or E alpha p). To distinguish between these possible genotypes these recombinants were crossed to B10.A(4R), which carries a functional E alpha k gene but is I-E-negative due to a nonexpressed E alpha b gene. F1 mice were examined for transcomplementing I-E molecules by immunoprecipitation of 3H-leucine-radiolabeled detergent lysates of spleen cells with a monoclonal I-E antibody (14-4-4). Detection of a transcomplementing I-E molecule was confirmed by immunoprecipitation with a monoclonal antibody (H9-14.8) specific for the I-Ek beta polypeptide chain derived from B10.A(4R) and by tryptic peptide map comparisons. Five recombinant mouse strains were able to complement with B10.A(4R) in F1 mice to generate a transcomplementing I-E molecule, and thus have an expressed I-E alpha gene (E alpha k or E alpha p). Four recombinants did not complement with B10.A(4R) in the F1 expression of I-E molecules, and thus have nonexpressed I-E alpha genes (E alpha f or E alpha q).

Animals↗
PubMed1988

A map of VH genes located next to the DH region in the Igh locus of two congenic Igh-recombinant mouse strains.

A new congenic mouse strain (C57BL/6-Igh-Vb-Ca) with a recombinant chromosome 12 is described. It carries the Igh-1a allele, but shows the serological characteristics of C57BL/6 when analyzed for idiotype expression with respect to the antigens dextran and (4-hydroxy-5-iodo-3-nitrophenyl)acetyl (NIP). We analyzed liver DNA from one animal for restriction fragment length polymorphism by hybridization to probes detecting members of nine VH gene families and DH segments, and compared it to DNA from animals carrying the nonrecombinant haplotypes Igha and Ighb, respectively. The breakpoint of recombination maps to the region carrying members of VH gene families VGAM3.8, PC7183 and Q52. The CB8KN strain which according to the serological analysis carries a recombinant Igh locus (Igh-Va-Cb) on BALB/c background was also analyzed. In this strain the breakpoint of recombination again maps to the region carrying members of VH gene families VGAM3.8, PC7183 and Q52. Our results show that the VH genes of families PC7183 and Q52 are interspersed and map to the region next to the DH locus. At least one gene from the VGAM3.8 family also maps to this region in the Igha and the Ighb haplotype.

Animals↗
PubMed1989

Autoimmune disease and cochlear pathology in the C3H/lpr strain mouse.

The C3H/lpr autoimmune strain mouse is a model for spontaneous systemic lupus erythematosus. Inner ear structure and function were examined during systemic autoimmune disease progression to identify correlated auditory system pathology. Onset of the systemic disease occurred at 2-3 months of age and was characterized by elevated serum immune complexes, cryoglobulins, and antinuclear antibodies. Coincident with the onset of autoimmune disease was degeneration of the stria vascularis. Early edema of the stria occurred in the apex and progressed basalward with duration of the disease. By 10 months of age, stria vascularis area was smaller and auditory brainstem response thresholds were elevated. No degeneration of hair cells was seen at any age, suggesting that the stria vascularis may be the primary anatomic site of autoimmune auditory damage in this mouse model.

Age Factors↗