{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T07:28:02Z","timestamp":1782286082974,"version":"3.54.5"},"reference-count":45,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2013,2,27]],"date-time":"2013-02-27T00:00:00Z","timestamp":1361923200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Vet Pathol"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:p>\n                    Salmonella enterica serovar Typhimurium ( S. Typhimurium) causes systemic inflammatory disease in mice by colonizing cells of the mononuclear leukocyte lineage. Mouse strains resistant to S. Typhimurium, including Sv129S6, have an intact Nramp1 ( Slc11a1) allele and survive acute infection, whereas C57\/BL6 mice, homozygous for a mutant Nramp1 allele, Nramp1\n                    <jats:sup>G169D<\/jats:sup>\n                    , develop lethal infections. Restoration of Nramp1 (C57\/BL6 Nramp1\n                    <jats:sup>G169<\/jats:sup>\n                    ) reestablishes resistance to S. Typhimurium; mice survive at least 3 to 4 weeks postinfection. Since many transgenic mouse strains are on a C57\/BL6 genetic background, C57\/BL6 Nramp1\n                    <jats:sup>G169<\/jats:sup>\n                    mice provide a model to examine host genetic determinants of resistance to infection. To further evaluate host immune response to S. Typhimurium, we performed comparative analyses of Sv129S6 and C57\/BL6 Nramp1\n                    <jats:sup>G169<\/jats:sup>\n                    mice 3 weeks following oral S. Typhimurium infection. C57\/BL6 Nramp1\n                    <jats:sup>G169<\/jats:sup>\n                    mice developed more severe inflammatory disease with splenic bacterial counts 1000-fold higher than Sv129S6 mice and relatively greater splenomegaly and blood neutrophil and monocyte counts. Infected C57\/BL6 Nramp1\n                    <jats:sup>G169<\/jats:sup>\n                    mice developed higher proinflammatory serum cytokine and chemokine responses (interferon-\u03b3, tumor necrosis factor\u2013\u03b1, interleukin [IL]\u20131\u03b2, and IL-2 and monocyte chemotactic protein\u20131 and chemokine [C-X-C motif] ligand 1, respectively) and marked decreases in anti-inflammatory serum cytokine concentrations (IL-10, IL-4) compared with Sv129S6 mice postinfection. Splenic dendritic cells and macrophages in infected compared with control mice increased to a greater extent in C57\/BL6 Nramp1\n                    <jats:sup>G169<\/jats:sup>\n                    mice than in Sv129S6 mice. Overall, data show that despite the Nramp1 gene present in both strains, C57\/BL6 Nramp1\n                    <jats:sup>G169<\/jats:sup>\n                    mice develop more severe, Th1-skewed, acute inflammatory responses to S. Typhimurium infection compared with Sv129S6 mice. Both strains are suitable model systems for studying inflammation in the context of adaptive immunity.\n                  <\/jats:p>","DOI":"10.1177\/0300985813478213","type":"journal-article","created":{"date-parts":[[2013,2,28]],"date-time":"2013-02-28T20:07:32Z","timestamp":1362082052000},"page":"867-876","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":49,"title":["<i>Salmonella enterica<\/i>\n                    Causes More Severe Inflammatory Disease in C57\/BL6\n                    <i>\n                      Nramp1\n                      <sup>G169<\/sup>\n                    <\/i>\n                    Mice Than Sv129S6 Mice"],"prefix":"10.1177","volume":"50","author":[{"given":"D. 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