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  • 18th International Mouse Genome Conference (2004)
    Pasteur Paris France Characterizing genes of susceptibility to complex disorders is one of the most promising challenges at the beginning of the XXI century The demyelinating disease induced by the persistent infection of Theiler s virus in the mouse spinal cord is studied as a model for Multiple Sclerosis Susceptibility to the infection amongst mouse strains depends mainly to the ability of their immune system to eliminate the virus By crossing and analyzing congenic strains between the SJL J and the B10 S strains two loci of susceptibility named Tmevp2 and Tmevp3 were located on chromosome 10 close to the Ifng gene We decided to characterize the Tmevp3 locus A cluster of cytokines containing at least 3 genes Tmevpg1 Ifng and Il Tif IL22 is an interesting region located at the telomeric part of the Tmevp3 interval since major loci of susceptibility between the SJL J and the B10 S are expressed in the immune system We decided to test this hypothesis by haplotyping this cluster in 15 strains 11 laboratory strains with known susceptibility to the persistence of Theiler s virus and 4 wild type derived strains We searched for polymorphism located in Tmevpg1 Ifng Il22 and Mdm1 Mdm2

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file141.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    a key interface between cells of the host and all classes of microbial pathogen By sensing nucleic acids the endosomal TLRs 3 7 and 9 play a particularly important role in the detection of viral infection and permit the host to mount an immediate and efficacious anti viral response In an effort to identify novel components of the TLR signaling apparatus we have pursued a program of germline saturation mutagenesis with N ethyl N nitrosourea ENU in mice The germline mutants are produced on the C57BL 6 background and peritoneal macrophages from individual animals are screened for their competence to respond to TLR dependent microbial inducers A strong phenodeviant called 3d was identified in the F3 generation as a non responder to nucleoside based molecules such as unmethylated CpG oligodeoxynucleotides Resiquimod a drug of the imidazoquinoline class and Poly I C TNF production induced by TLRs 3 7 and 9 was completely prevented in 3d homozygotes However heterozygotes were unaffected and the ability to produce TNF in response to other bacterial compounds sensed by TLRs 1 2 4 and 6 was intact 3d homozygotes show extreme susceptibility to infection by mouse cytomegalovirus MCMV infection in vivo After IP inoculation with

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file142.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    1 Tabeta K 1 Mudd S 1 Sovath S 1 Shamel L 1 Hartung T 2 Zahringer U 3 Beutler B 1 1 The Scripps Research Institue La Jolla United States 2 Department of Biochemical Pharmacology University of Konstanz Konstanz Germany 3 Research Center Borstel Leipniz center for Medicine and Bioscience Borstel Germany The mammalian Toll like receptors TLRs activate cells of the innate immune system when stimulated by diverse ligands of microbial origin In some instances these ligands are directly engaged by the TLRs however this is not necessarily true in all cases TLR2 recognizes multiple structurally disparate microbial ligands consistent with a requirement for co receptors in ligand binding Using N ethyl N nitrosourea ENU we generated the recessive immunodeficiency phenotype oblivious in which macrophages show diminished awareness of the S enantiomer of the di acylated bacterial lipopeptide MALP 2 and lipoteichoic acid LTA together with an increased susceptibility to Staphylococcus aureus infection Oblivious macrophages readily detect the tri acylated bacterial lipopeptide PAM 3 CSK 4 as well as zymosan revealing that some TLR2 ligands are activated via an Oblivious independent pathway The gene responsible for the oblivious phenotype has been positionally cloned and was proven to result

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file143.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    people the incidence of human adenovirus disease is increasing with the increased number of immunosuppressed patients particularly pediatric bone marrow transplant recipients Identifying host factors involved in susceptibility to adenovirus infections is thus of importance in transplantation and also because of projected uses of adenovirus vectors in cancer treatments Study of human adenoviruses in animal hosts is not possible due to the species specific nature of adenoviruses MAV 1 is an excellent model for studying susceptibility because there are significant differences in susceptibility to MAV 1 in different inbred mouse strains SJL J mice are susceptible to MAV 1 succumbing to a low dose infection 8 10 days post infection with high virus loads in the brain and with a 50 lethal dose LD 50 more than 4 log units lower than other strains of mice including C3H HeJ BALB cJ 129 SvEv and C57BL 6J 1 When resistant mice are sublethally irradiated they become susceptible to MAV 1 infection Primary embryo fibroblasts and primary peritoneal macrophages from resistant and susceptible mice produce equal yields of MAV 1 when infected in culture These data suggest that systemic factors such as components of the innate or adaptive immune system play a

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file144.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    International Livestock Research Institute ILRI Nairobi Kenya 2 University of Liverpool Liverpool United Kingdom 3 University of New England Armidale Australia Different inbred mouse strains show significant differences in innate resistance to Trypanosoma congolense infection A J mice are highly susceptible and C57BL 6 mice are relatively resistant while BALB C mice are intermediate We investigated the development of pathology during the acute phase of trypanosome infection in these three strains A total of 240 mice of A J C57BL 6 and BALB C were challenged with 10 4 blood stream form of T congolense IL 1180 parasite At day 0 3 5 7 9 13 and 17 post infection the body weight skin temperature and parasitaemia were recorded At each collection point 30 mice were sacrificed and the spleen liver and kidney were examined and weighed On day 3 and 13 there was a significant drop in the skin temperature in all the strains This drop corresponds to the first parasitaemia and the peak of infection respectively On day 3 the associated gross pathology showed a marginally enlarged spleen 140 but no changes were observed on the liver and kidney On day 13 the spleen increased twelve fold while

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file145.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    ILRI Nairobi Kenya 2 University of Liverpool Liverpool United Kingdom 3 University of New England Armidale Australia The A J A mouse strain is more susceptible to infection with African trypanosomes and die earlier than the more resistant C57BL 6 BL6 mice while BALB c BALB is known to be intermediately susceptible In an early study trypanotolerance QTL associated with survival time following infection with the disease were mapped to chromosomes 17 5 and 1 using two F 2 resource populations C57BL 6 x A J and C57BL 6 x BALB c and designated as Tir1 Tir2 and Tir3 respectively Subsequently these QTL were fine mapped using F 6 advanced intercross line AIL populations After infections with Trypanosoma congolense A J mice developed a higher parasitemia than BL6 mice In contrast the BL6 mice never develop such high parasitemia but start dying in late stages of the infection Searching for more parameters which might underline the variation in susceptibility of the different mouse strains we recorded the kinetics of anemia development in the three mouse strains following infection with T congolense BL6 mice developed anemia within a week after infection and this lack of red blood cells got more severe

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file146.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    WITH PLASMODIUM CHABAUDI CHABAUDI 408XZ Hernandez M 1 Naessens J 1 Musoke A 1 Rihet P 3 Ole MoiYoi O 2 Iraqi F 1 1 International Livestock Research Institute ILRI Nairobi Kenya 2 Institute of Molecular and Cell Biology of Africa IMCBA Nairobi Kenya 3 Université de la Méditerranée Marseille France Tumour necrosis factor α TNFa plays a pleiotropic role during the murine malarial infection It is involved in controlling the blood parasitaemia levels as well as the mortality rates of the host Membrane bound TNFa is involved in the most severe form of the disease the cerebral malaria Some studies have correlated TNFa with hypothermia hyperlactataemia hypoglycaemia and a suppression of the erythropoietic responses although others have not supported the role of TNFa in the two latter clinical aspects We have studied several parameters of pathology in TNFa C57BL 6J and TNFa C57BL 6J mice after infection with Plasmodium chabaudi adami 408XZ Results have shown that blood glucose and lactate levels and body weight are not significantly different between TNFa C57BL 6J and TNFa C57BL 6J mice during infection However TNFa C57BL 6J mice significantly suffered a more severe anaemia and hypothermia than TNFa C57BL 6J mice In our

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file147.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    have been mapped to chromosome 1 5 and 17 and named Tir1 2 and 3 Tir2 QTL has been fine mapped to less than 1cM using F 13 advanced intercross lines The particular Tir2 region spanning 2KB on the mouse genome was examined for possible candidate genes Plausible candidate genes in the locus included toll like receptor 1 TLR1 and TLR6 among others Rapid defense mechanisms are provided through recognition of pathogen associated molecular patterns by TLRs Their expression and cooperation is essential for the induction of interleukins through their interaction with membrane glycosylphosphatidylinositol GPI anchors Spleen and liver tissues were collected at day 0 4 7 and 10 post infection from 4 groups of each of the resistant C57BL 6J and susceptible AJ mice Tissue specific expression levels of each of the two genes was determined using a semi quantitative RT PCR Analysis of variance of the mean ratios of ß actin as the house keeping gene with each of the two genes revealed that the genes are regulated in a statistically significant fashion The level of TLR1 increased between day 4 and day 7 in the resistant C57BL 6J while it declined in the susceptible strain over the

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file148.shtml (2016-02-17)
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