{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T17:11:40Z","timestamp":1793725900439,"version":"4.6.1"},"reference-count":44,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2003,2,1]],"date-time":"2003-02-01T00:00:00Z","timestamp":1044057600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2003,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Brucella,<\/jats:italic>the causative agent of brucellosis in animals and humans, can survive and proliferate within macrophages. Macrophages mediate mouse resistance to various pathogens through the expression of the<jats:italic>Nramp1<\/jats:italic>gene. The role of this gene in the control of<jats:italic>Brucella<\/jats:italic>infection was investigated. When BALB\/c mice (<jats:italic>Nramp1<jats:sup>s<\/jats:sup><\/jats:italic>) and C.CB congenic mice (<jats:italic>Nramp1<jats:sup>r<\/jats:sup><\/jats:italic>) were infected with<jats:italic>Brucella melitensis,<\/jats:italic>the number of<jats:italic>Brucella<\/jats:italic>organisms per spleen was significantly larger in the C.CB mice than in the BALB\/c mice during the first week postinfection (p.i.). This<jats:italic>Nramp1<\/jats:italic>-linked susceptibility to<jats:italic>Brucella<\/jats:italic>was temporary, since similar numbers of<jats:italic>Brucella<\/jats:italic>were recovered from the two strains of mice 2 weeks p.i. The effect of<jats:italic>Nramp1<\/jats:italic>expression occurred within splenocytes intracellularly infected by<jats:italic>Brucella.<\/jats:italic>However, there was no difference between in vitro replication rates of<jats:italic>Brucella<\/jats:italic>in macrophages isolated from the two strains of mice infected in vivo or in<jats:italic>Nramp1<\/jats:italic>RAW264 transfectants. In mice, infection with<jats:italic>Brucella<\/jats:italic>induced an inflammatory response, resulting in splenomegaly and recruitment of phagocytes in the spleen, which was amplified in C.CB mice. Reverse transcription-PCR (RT-PCR), performed 5 days p.i., showed that inducible nitric oxide synthase, tumor necrosis factor alpha (TNF-\u03b1), interleukin-12 p40 (IL-12p40), gamma interferon (IFN-\u03b3), and IL-10 mRNAs were similarly induced in spleens of the two strains. In contrast, the mRNA of KC, a C-X-C chemokine, was induced only in infected C.CB mice at this time. This pattern of mRNA expression was maintained at 14 days p.i., with IFN-\u03b3 and IL-12p40 mRNAs being more intensively induced in the infected C.CB mice, but TNF-\u03b1 mRNA was no longer induced. The higher recruitment of neutrophils observed in the spleens of infected C.CB mice could explain the temporary susceptibility of C.CB mice to<jats:italic>B. melitensis<\/jats:italic>infection. In contrast to infections with<jats:italic>Salmonella, Leishmania,<\/jats:italic>and<jats:italic>Mycobacterium,<\/jats:italic>the expression of the<jats:italic>Nramp1<\/jats:italic>gene appears to be of limited importance for the natural resistance of mice to<jats:italic>Brucella<\/jats:italic>.<\/jats:p>","DOI":"10.1128\/iai.71.2.621-628.2003","type":"journal-article","created":{"date-parts":[[2003,1,22]],"date-time":"2003-01-22T23:03:20Z","timestamp":1043276600000},"page":"621-628","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":20,"title":["Nramp1 Is Not a Major Determinant in the Control of<i>Brucella melitensis<\/i>Infection in Mice"],"prefix":"10.1128","volume":"71","author":[{"given":"Laurence A.","family":"Guilloteau","sequence":"first","affiliation":[{"name":"Pathologie Infectieuse et Immunologie"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacques","family":"Dornand","sequence":"additional","affiliation":[{"name":"Institut National de la Sante\u0301 et de la Recherche Me\u0301dicale U-431, Montpellier, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antoine","family":"Gross","sequence":"additional","affiliation":[{"name":"Institut National de la Sante\u0301 et de la Recherche Me\u0301dicale U-431, Montpellier, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michel","family":"Olivier","sequence":"additional","affiliation":[{"name":"Pathologie Infectieuse et Immunologie"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabienne","family":"Cortade","sequence":"additional","affiliation":[{"name":"Pathologie Infectieuse et Immunologie"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yves Le","family":"Vern","sequence":"additional","affiliation":[{"name":"Service commun de cytome\u0301trie en flux, Institut National de la Recherche Agronomique, Nouzilly"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dominique","family":"Kerboeuf","sequence":"additional","affiliation":[{"name":"Service commun de cytome\u0301trie en flux, Institut National de la Recherche Agronomique, Nouzilly"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.20506\/rst.17.1.1085"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2567.1999.00672.x"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.69.5.3110-3119.2001"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200107)31:7<2060::AID-IMMU2060>3.0.CO;2-L"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(00)00295-1"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1462-5822.2001.00150.x"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-1157(76)80019-4"},{"key":"e_1_3_2_9_2","first-page":"153","volume":"13","year":"1982","unstructured":"Bosseray, N., M. 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