Genetics of Resistance to Infection with Salmonella typhimurium in Mice

Plant, Janet E.; Glynn, A. A.

doi:10.1093/infdis/133.1.72

Cited by 303 publications

(168 citation statements)

References 12 publications

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“…[25][26][27][28] It was recognized over 30 years ago that the susceptibility of inbred mice to infection with virulent Salmonella Typhimurium varied from strain to strain and that these differences were genetically controlled. 29,30 In general, classical inbred strains of mice can be classified into three distinct categories in regard to their susceptibility to Salmonella. 20,30 129S6/SvEvTac mice are extremely resistant to infection with Salmonella Typhimurium compared to A/J mice that present an intermediate susceptibility phenotype and show increased survival time with decreasing infectious dose but cannot survive the infection (Figure 2).…”

Section: Mouse Model Of Salmonella Typhimurium Infectionmentioning

confidence: 99%

“…29 In this early paper, the authors showed that eight strains of inbred mice fell into two sharply defined groups with respect to resistance to infection. Four strains (CBA, A/J, C3H/He and DBA/2) were resistant (LD 50 410 5 ) to Salmonella Typhimurium C5 and the other four strains (BALB/c, C57BL, B10.D2 and DBA/1) were susceptible (LD 50 o10).…”

Section: Nramp1mentioning

confidence: 99%

“…40 The resistance allele is dominant and influences the rate of bacterial growth during the exponential phase of multiplication in the RES and the LD 50 after lethal challenge with high doses of Salmonella Typhimurium. 29 Ity is expressed by macrophages and Ity r confers an increased bactericidal capacity to this cell type in comparison to Ity s . 47 Studies involving an experimental mouse model of infection with Mycobacteria and L. donovani showed that Bcg r and Lsh r behaved similarly, being expressed in macrophages and conferring resistance to bacterial multiplication of the intracellular parasites during the early phase of infection.…”

Section: Nramp1mentioning

confidence: 99%

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Genetic regulation of host responses to Salmonella infection in mice

Malo

2002

Genes Immun

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Salmonella spp are Gram-negative bacteria capable of infecting a wide range of host species, including humans, domesticated and wild mammals, reptiles, birds and insects. The outcome of an encounter between Salmonella and its host is dependent upon multiple factors including the host genetic background. To facilitate the study of the genetic factors involved in resistance to this pathogen, mouse models of Salmonella infection have been developed and studied for years, allowing identification of several genes and pathways that may influence the disease outcome. In this review, we will cover some of the genes involved in mouse resistance to Salmonella that were identified through the study of congenic mouse strains, cloning of spontaneous mouse mutations, use of site-directed mutagenesis or quantitative trait loci analysis. In parallel, the relevant information pertaining to genes involved in resistance to Salmonella in humans will be discussed.

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Section: Mouse Model Of Salmonella Typhimurium Infectionmentioning

confidence: 99%

Section: Nramp1mentioning

confidence: 99%

Section: Nramp1mentioning

confidence: 99%

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Genetic regulation of host responses to Salmonella infection in mice

Malo

2002

Genes Immun

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“…The parental strains are known to differ in response to many pathogens. [26][27][28][29] The other notable advantage of this particular panel of RI strains is that both parental strains have been sequenced. 30 This makes it possible to use reverse genetic methods to test modifier genes.…”

Section: Introductionmentioning

confidence: 99%

Susceptibility to severe streptococcal sepsis: use of a large set of isogenic mouse lines to study genetic and environmental factors

et al. 2007

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Variation in responses to pathogens is influenced by exposure history, environment and the host's genetic status. We recently demonstrated that human leukocyte antigen class II allelic differences are a major determinant of the severity of invasive group A streptococcal (GAS) sepsis in humans. While in-depth controlled molecular studies on populations of genetically wellcharacterized humans are not feasible, it is now possible to exploit genetically diverse panels of recombinant inbred BXD mice to define genetic and environmental risk factors. Our goal in this study was to standardize the model and identify genetic and nongenetic covariates influencing invasive infection outcomes. Despite having common ancestors, the various BXD strains (n strains ¼ 33, n individuals ¼ 445) showed marked differences in survival. Mice from all strains developed bacteremia but exhibited considerable differences in disease severity, bacterial dissemination and mortality rates. Bacteremia and survival showed the expected negative correlation. Among nongenetic factors, age -but not sex or weight -was a significant predictor of survival (P ¼ 0.0005). To minimize nongenetic variability, we limited further analyses to mice aged 40-120 days and calculated a corrected relative survival index that reflects the number of days an animal survived post-infection normalized to all significant covariates. Genetic background (strain) was the most significant factor determining susceptibility (Pp0.0001), thus underscoring the strong effect of host genetic variation in determining susceptibility to severe GAS sepsis. This model offers powerful unbiased forward genetics to map specific quantitative trait loci and networks of pathways modulating the severity of GAS sepsis.

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“…35,36 Nramp1 is a major determinant of innate host resistance to infection. The gene affects intracellular replication of a wide range of pathogens including S. typhimurium, 37 Leishmania donovani, 38 M. lepraemurium, 39 M. intracellulare, 40 M. avium, 41 and the TB vaccine strain M. bovis -Bacillus Calmette-Guérin (BCG). 42 Specifically, a glycine-to-aspartic-acid change at amino acid 169 (G169D), located in the predicted transmembrane domain number 4 (TM 4), has removed the host's ability to inhibit pathogen growth.…”

Section: Discussionmentioning

confidence: 99%

NRAMP1 is not associated with asthma, atopy, and serum immunoglobulin E levels in the French Canadian population

et al. 2005

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Reduced infection by mycobacteria, including Mycobacterium tuberculosis, may be partly responsible for increased prevalence of allergic and autoimmune diseases in developed countries. In a murine model of innate resistance to mycobacteria, the Nramp1 gene has been shown to affect asthma susceptibility. From this observation, it was proposed that human NRAMP1 may be a modulator of asthma risk in human populations. To experimentally test the candidacy of NRAMP1 in asthma susceptibility, we characterized five genetic variants of NRAMP1 (5 0 CA n , 274C4T, 469 þ 14G4C, D543N, and 1729 þ del4) in an asthma family-based cohort from northeastern Quebec. We did not observe any significant association between NRAMP1 variants (either allele or haplotype specific) with asthma, atopy, or serum immunoglobulin E levels. These results demonstrate that, in spite of direct involvement of Nramp1 in a murine asthma model, in human populations NRAMP1 is not likely to be a major contributor to the genetic etiology of asthma and asthma-related phenotypes.

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Genetics of Resistance to Infection with Salmonella typhimurium in Mice

Cited by 303 publications

References 12 publications

Genetic regulation of host responses to Salmonella infection in mice

Genetic regulation of host responses to Salmonella infection in mice

Susceptibility to severe streptococcal sepsis: use of a large set of isogenic mouse lines to study genetic and environmental factors

NRAMP1 is not associated with asthma, atopy, and serum immunoglobulin E levels in the French Canadian population

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