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

Blanchet, Charlène; Jaubert, Jean; Carniel, Élisabeth; Fayolle, Corinne; Milon, Geneviève; Szatanik, Marek; Panthier, Jean‐Jacques; Montagutelli, Xavier

doi:10.1038/gene.2010.45

Cited by 17 publications

(40 citation statements)

References 38 publications

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“…A recent study using fully virulent plague pathogens found that multiple loci were required for mice to survive in a Y. pestis subcutaneous infection model (32)(33)(34) (12), and DBA2/J mice (M. Tencati and R. Tapping, unpublished data). The resistance in BALB/cJ mice has been localized to chromosome 17, whereas at least part of the resistance in 129 mice localizes to chromosome 1.…”

Section: Discussionmentioning

confidence: 99%

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

Tencati

Tapping

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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Section: Discussionmentioning

confidence: 99%

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

Tencati

Tapping

2016

Infect Immun

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“…The SEG/Pas strain of Mus spretus is highly resistant to pigmentation-positive Y. pestis (2). Multiple alleles that contributed to resistance in SEG/Pas mice were discovered (2). The mean times of death of SEG/Pas mice and C57BL/6 mice were similar (2).…”

mentioning

confidence: 68%

“…Plague resistance has also been seen in another mouse species. The SEG/Pas strain of Mus spretus is highly resistant to pigmentation-positive Y. pestis (2). Multiple alleles that contributed to resistance in SEG/Pas mice were discovered (2).…”

mentioning

confidence: 99%

“…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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confidence: 99%

“…The mean times of death of SEG/Pas mice and C57BL/6 mice were similar (2). Blanchet et al suggested that the mechanism of resistance related to an early response to infection (2).…”

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confidence: 99%

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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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Genetic variation at the MHC DRB1 locus is similar across Gunnison's prairie dog (Cynomys gunnisoni) colonies regardless of plague history

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Califf

Stone

et al. 2016

Ecology and Evolution

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Yersinia pestis was introduced to North America around 1900 and leads to nearly 100% mortality in prairie dog (Cynomys spp.) colonies during epizootic events, which suggests this pathogen may exert a strong selective force. We characterized genetic diversity at an MHC class II locus (DRB1) in Gunnison's prairie dog (C. gunnisoni) and quantified population genetic structure at the DRB1 versus 12 microsatellite loci in three large Arizona colonies. Two colonies, Seligman (SE) and Espee Ranch (ES), have experienced multiple plague‐related die‐offs in recent years, whereas plague has never been documented at Aubrey Valley (AV). We found fairly low allelic diversity at the DRB1 locus, with one allele (DRB1*01) at high frequency (0.67–0.87) in all colonies. Two other DRB1 alleles appear to be trans‐species polymorphisms shared with the black‐tailed prairie dog (C. ludovicianus), indicating that these alleles have been maintained across evolutionary time frames. Estimates of genetic differentiation were generally lower at the MHC locus (F ST = 0.033) than at microsatellite markers (F ST = 0.098). The reduced differentiation at DRB1 may indicate that selection has been important for shaping variation at MHC loci, regardless of the presence or absence of plague in recent decades. However, genetic drift has probably also influenced the DRB1 locus because its level of differentiation was not different from that of microsatellites in an F ST outlier analysis. We then compared specific MHC alleles to plague survivorship in 60 C. gunnisoni that had been experimentally infected with Y. pestis. We found that survival was greater in individuals that carried at least one copy of the most common allele (DRB1*01) compared to those that did not (60% vs. 20%). Although the sample sizes of these two groups were unbalanced, this result suggests the possibility that this MHC class II locus, or a nearby linked gene, could play a role in plague survival.

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

Cited by 17 publications

References 38 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

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

Genetic variation at the MHC DRB1 locus is similar across Gunnison's prairie dog (Cynomys gunnisoni) colonies regardless of plague history

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