Mice Naturally Resistant to
            <i>Yersinia pestis</i>
            Δ
            <i>pgm</i>
            Strains Commonly Used in Pathogenicity Studies

Congleton, Yasemin H. K.; Wulff, Christine; Kerschen, E. J.; Straley, Susan C.

doi:10.1128/iai.00597-06

Cited by 15 publications

(19 citation statements)

References 12 publications

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“…We therefore chose to use inbred mice as a model to identify genes that may confer resistance against plague. We and others subsequently identified several inbred strains of mice that are resistant (11)(12)(13)(14). Resistance of the 129 line was first identified by Congleton et al in a pigmentation locus-negative (pgm Ϫ ) infection model of plague (11) but not for a fully virulent Y. pestis strain.…”

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confidence: 99%

“…We and others subsequently identified several inbred strains of mice that are resistant (11)(12)(13)(14). Resistance of the 129 line was first identified by Congleton et al in a pigmentation locus-negative (pgm Ϫ ) infection model of plague (11) but not for a fully virulent Y. pestis strain. The resistance is observed in multiple substrains of this line, and further studies by our laboratory have localized a major portion of the resistance phenotype to chromosome 1.…”

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confidence: 99%

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Resistance of Mice of the 129 Background to Yersinia pestis Maps to Multiple Loci on Chromosome 1

Tencati

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2016

Infect Immun

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Yersinia pestis is a Gram-negative bacterium that is the causative agent of bubonic and pneumonic plague. It is commonly acquired by mammals such as rodents and humans via the bite of an infected flea. We previously reported that multiple substrains of the 129 mouse background are resistant to pigmentation locus-negative (pgm ؊ ) Yersinia pestis and that this phenotype maps to a 30-centimorgan (cM) region located on chromosome 1. In this study, we have further delineated this plague resistance locus to a region of less than 20 cM through the creation and phenotyping of recombinant offspring arising from novel crossovers in this region. Furthermore, our experiments have revealed that there are at least two alleles in this initial locus, both of which are required for resistance on a susceptible C57BL/6 background. These two alleles work in trans since resistance is restored in offspring possessing one allele contributed by each parent. Our studies also indicated that the Slc11a1 gene (formerly known as Nramp1) located within the chromosome1 locus is not responsible for conferring resistance to 129 mice.

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Resistance of Mice of the 129 Background to Yersinia pestis Maps to Multiple Loci on Chromosome 1

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2016

Infect Immun

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“…Differences in susceptibility to Y. pestis have been recently reported between laboratory inbred strains of mice, 8 including the mapping of two resistance alleles, close to the interleukin-10 gene (chromosome 1) 9 and histocompatibility complex (chromosome 17). 10 These results were obtained upon intravenous injection of the Y. pestis mutant strain KIM5, which lacks the chromosomal pgm locus.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, the relevance of these results to natural infection in animals and humans is limited, as the same inbred strains of mice are susceptible to virulent Y. pestis strains. 8 All classical laboratory strains (such as C57BL/6 (B6)) are susceptible to subcutaneous (s.c.) injection of the fully virulent Y. pestis strain C092, an experimental setting designed to mimic many features of natural exposure. 11 In this study, we report that the SEG/Pas (SEG) inbred strain, which was established from Mus spretus progenitors, exhibits a high level of resistance under the same conditions.…”

Section: Introductionmentioning

confidence: 99%

Mus spretus SEG/Pas mice resist virulent Yersinia pestis, under multigenic control

et al. 2010

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Laboratory mice are well known to be highly susceptible to virulent strains of Yersinia pestis in experimental models of bubonic plague. We have found that Mus spretus-derived SEG/Pas (SEG) mice are exceptionally resistant to virulent CO92 and 6/69 wild type strains. Upon subcutaneous injection of 10 2 colony-forming units (CFU), 90% of females and 68% of males survived, compared with only an 8% survival rate for both male and female C57BL/6 mice. Furthermore, half of the SEG mice survived a challenge of up to 10 7 CFU. The time required for mortality was similar between B6 and SEG, suggesting that survival is dependent on early rather than late processes. The analysis of 322 backcross mice identified three significant quantitative trait loci (QTLs) on chromosomes 3, 4 and 6, with dominant SEG protective alleles. Each QTL increased the survival rate by approximately 20%. The three QTLs function additively, thereby accounting for 67% of the difference between the parental phenotypes. Mice heterozygous for the three QTLs were just as resistant as SEG mice to Y. pestis challenge. The SEG strain therefore offers an invaluable opportunity to unravel mechanisms and underlying genetic factors of resistance against Y. pestis infection.

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“…Several laboratories (2,8,41,42) have reported different mouse strains intrinsically resistant to plague. Resistance does not appear to be conferred by one specific strain or genetic background.…”

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Resistance to Yersinia pestis Infection Decreases with Age in B10.T(6R) Mice

et al. 2011

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We demonstrate that 2-month-old female B10.T(6R) mice are highly resistant to systemic infection with the KIM5 strain of Yersinia pestis and that B10.T(6R) mice become susceptible to Y. pestis infection by the age of 5 months. In this study, young (2-month-old) and middle-aged (5-to 12-month-old) B10.T(6R) mice were infected with equal CFU counts of Y. pestis. The 50% lethal dose (LD 50 ) for young B10.T(6R) mice was ϳ1.4 ؋ 10 4 CFU, while middle-aged B10.T(6R) mice exhibited an LD 50 of ϳ60 CFU. Elevated bacterial burdens were found in the spleens of middle-aged mice at 24 and 60 h and in the livers at 60 h postinfection. Immune cell infiltration was greater in the livers of resistant young mice than in those of middle-aged mice and mice of the susceptible C57BL/6N strain. Unlike susceptible mice, young B10.T(6R) mice did not develop necrotic lesions throughout the liver. Instead, livers from young B10.T(6R) mice contained granuloma-like structures. Immunohistochemical staining of liver sections from these mice at 60 h postinfection revealed that the majority of immune cells present in these structures were neutrophils. These findings suggest that resistance to plague in B10.T(6R) mice correlates with early formation of neutrophilic lesions in the liver.

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Mice Naturally Resistant to Yersinia pestis Δ pgm Strains Commonly Used in Pathogenicity Studies

Cited by 15 publications

References 12 publications

Resistance of Mice of the 129 Background to Yersinia pestis Maps to Multiple Loci on Chromosome 1

Resistance of Mice of the 129 Background to Yersinia pestis Maps to Multiple Loci on Chromosome 1

Mus spretus SEG/Pas mice resist virulent Yersinia pestis, under multigenic control

Resistance to Yersinia pestis Infection Decreases with Age in B10.T(6R) Mice

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