Genetic determinants of acute inflammation regulate Salmonella infection and modulate Slc11a1 gene (formerly Nramp1) effects in selected mouse lines

Borrego, Andrea; Peters, L C; Jensen, José Ricardo; Ribeiro, Orlando; Cabrera, Wafa Hanna Koury; Starobinas, Nancy; Séman, Michel; Ibañez, Olga M.; Franco, Marcelo De

doi:10.1016/j.micinf.2006.08.005

Cited by 33 publications

(67 citation statements)

References 31 publications

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“…1 Although the exact SNPs underlying such differential responsiveness are under investigation, one genetic variation involved in the control of immune inflammatory reactions between AIRmin and AIRmax strains is well known and involves the gene SLC11A1 (NRAMP1). 28,37 Interestingly, SNPs in SLC11A1 have been associated with the resistance/ susceptibility to human RA development, [38][39][40] but unfortunately no data regarding SLC11A1 association with human PD is available in the literature. Accordingly, with the shared genetic susceptibility hypothesis, preliminary data from our group 41 point to a significant higher frequency of the 3/3 genotype of SLC11A1 rs34448891 SNP (earlier associated to RA) 38 in chronic PD patients.…”

Section: Discussionmentioning

confidence: 99%

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Trombone¹,

Claudino²,

Colavite³

et al. 2010

Genes Immun

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Periodontitis (PD) and rheumatoid arthritis (RA) have been found to be clinically associated and to share the chronic nature of the inflammatory reaction associated with bone resorption activity. However, the mechanisms underlying such association are unknown. Therefore, we examined the basis of Actinobacillus actinomycetemcomitans-and Porphyromonas gingivalis-induced PD and pristane-induced arthritis (PIA) interaction in mice. Higher severity PD in the genetically inflammation prone acute inflammatory reactivity maximum (AIRmax) mice strain was associated with higher levels of TNF-a, IL-1b, IL-17, matrix metalloproteinase (MMP)-13, and RANKL, whereas PD/PIA co-induction resulted in even higher levels of IL-1b, IFN-g, IL-17, RANKL, and MMP-13 levels. Conversely, PD/PIA co-induction in AIRmin strain did not alter the course of both pathologies. PIA/PD co-induction resulted in altered expression of T-cell subsets transcription factors expression, with T-bet and RORg levels being upregulated, whereas GATA-3 levels were unaltered. Interestingly, PIA induction resulted in alveolar bone loss, such response being highly dependent on the presence of commensal oral bacteria. No differences were found in PIA severity parameters by PD co-induction. Our results show that the interaction between experimental PD and arthritis in mice involves a shared hyper-inflammatory genotype and functional interferences in innate and adaptive immune responses.

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Section: Discussionmentioning

confidence: 99%

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Trombone¹,

Claudino²,

Colavite³

et al. 2010

Genes Immun

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“…An additional Salmonella-related locus, modifier of Salmonella typhimurium susceptibility 4, has been mapped to this region and modulates acute inflammatory reactions. 22 We chose to further characterize the Ity2 locus because of the availability of congenic and subcongenic mice. We showed previously that the two regions within the Ity2 interval (Ity2A and Ity2B) were necessary for the resistance of B6.MOLF-Ity/Ity2 mice to infection on an Slc11a1-corrected C57BL/6J background.…”

Section: Discussionmentioning

confidence: 99%

Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2

et al. 2011

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Typhoid fever, which is caused by Salmonella typhi and paratyphi, is a severe systemic disease that remains a major public health issue in several areas of the world. We can model the human disease using mice infected with a related bacterium, Salmonella typhimurium. This model recapitulates several clinical aspects of the human disease and allows for the study of the host response to Salmonella typhimurium infection in vivo. Previous work in our laboratory has identified three Immunity to typhimurium loci (Ity, Ity2 and Ity3) in the wild-derived MOLF/Ei mice, influencing survival after infection with Salmonella typhimurium. The MOLF/Ei alleles at Ity and Ity2 are protective, while the MOLF/Ei allele at Ity3 confers susceptibility. In this paper, we have generated a novel cross combination between the highly susceptible strain, MOLF/Ei, and the resistant strain, 129S6, to better define the genetic architecture of susceptibility to infection in MOLF/Ei. Using this cross, we have replicated the locus on chr 11 (Ity2) and identified a novel locus on chr 13 (Ity13). Using microarrays and transcriptional profiling, we examined the response of uninfected and infected Ity2 congenic mice. These analyses demonstrate a role for both type-1-interferon (IFN) and TRP53 signaling in the pathogenesis of Salmonella infection.

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“…Because of this, the laboratory mouse has been the experimental model of choice to study pathogenesis of infection, including innate and acquired host defense mechanisms. Inbred mouse strains differ significantly in their degree of susceptibility to infection with various human bacterial (eg, Mycobacterium tuberculosis, 15,16 Salmonella enterica, 17 Streptococcus pyogenes, 18 Streptococcus pneumoniae 19 ), fungal (eg, Histoplasma capsulatum, 20 Aspergillus fumigatus 21 ), protozoan (eg, Leishmania major, 22 Plasmodium berghei, 23 Plasmodium chabaudi 24 ), helminthic (eg, Schistosoma mansoni 25,26 ) as well as viral (eg, respiratory syncytial virus 27,28 ) pathogens. This attribute has been exploited to identify novel loci influencing resistance/susceptibility to infection and to provide new insight on host mechanisms involved in response to those pathogens that ultimately affect the onset, progression, and outcome of the infection.…”

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confidence: 99%

Immunological Mechanisms Underlying the Genetic Predisposition to Severe Staphylococcus aureus Infection in the Mouse Model

Köckritz-Blickwede

Rohde

Oehmcke

et al. 2008

The American Journal of Pathology

122

130

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Host genetic variations play a significant role in conferring predisposition to infection. In this study, we examined the immune mechanisms underlying the host genetic predisposition to severe Staphylococcus aureus infection in different mouse strains. Whereas C57BL/6 mice were the most resistant in terms of control of bacterial growth and survival, A/J, DBA/2, and BALB/c mice were highly susceptible and succumbed to infection shortly after bacterial inoculation. Other strains (C3H/HeN, CBA, and C57BL/10) exhibited intermediate susceptibility levels. Susceptibility of mice to S. aureus was associated with an inability to limit bacterial growth in the kidneys and development of pathology. Resistance to S. aureus in C57BL/6 mice was dependent on innate immune mechanisms because Rag2-IL2R␥ ؊/؊ C57BL/6 mice, which are deficient in B, T, and NK cells, were also resistant to infection. Indeed, neutrophil depletion or inhibition of neutrophil recruitment rendered C57BL/6 mice completely susceptible to S. aureus, indicating that neutrophils are essential for the observed resistance. Although neutrophil function is not inhibited in A/J mice, expression of neutrophil chemoattractants KC and MIP-2 peaked earlier in the kidneys of C57BL/6 mice than in A/J mice, indicating that a delay in neutrophil recruitment to the site of infection may underlie the increased susceptibility of A/J mice to S.

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Genetic determinants of acute inflammation regulate Salmonella infection and modulate Slc11a1 gene (formerly Nramp1) effects in selected mouse lines

Cited by 33 publications

References 31 publications

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2

Immunological Mechanisms Underlying the Genetic Predisposition to Severe Staphylococcus aureus Infection in the Mouse Model

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