{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T15:51:13Z","timestamp":1791129073909,"version":"4.1.0"},"reference-count":48,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2009,7,1]],"date-time":"2009-07-01T00:00:00Z","timestamp":1246406400000},"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":[[2009,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Brucella abortus<\/jats:italic>is an intracellular pathogen that persists within phagocytic cells of the reticuloendothelial system. To identify in vivo interactions between<jats:italic>B. abortus<\/jats:italic>and the host that lead to persistent infection, we studied the persistence of<jats:italic>B. abortus<\/jats:italic>and an isogenic<jats:italic>virB<\/jats:italic>mutant deficient in the VirB type IV secretion system (T4SS) in knockout mice. In contrast to control mice, mice lacking B cells (<jats:italic>Igh6<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) were permissive for infection with the attenuated<jats:italic>virB<\/jats:italic>mutant. To determine the basis for this phenotype, we characterized immune functions of<jats:italic>Igh6<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice in the context of<jats:italic>B. abortus<\/jats:italic>infection.<jats:italic>Igh6<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice had greater numbers of extracellular bacteria in the spleen and increased early expression of proinflammatory cytokines during<jats:italic>B. abortus<\/jats:italic>infection. Further, a<jats:italic>virB<\/jats:italic>mutant, despite its wild-type level of survival, failed to elicit microgranuloma formation in the spleens of<jats:italic>Igh6<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice, suggesting a requirement for the T4SS to elicit this pathological change. Passive transfer of immunoglobulin G from nai\u0308ve mice restored the ability of<jats:italic>Igh6<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice to control the persistence of the<jats:italic>virB<\/jats:italic>mutant by a complement-independent mechanism. Further, adoptive transfer of CD11b<jats:sup>+<\/jats:sup>cells from C57BL\/6 mice to<jats:italic>Igh6<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice restored the ability of the knockout mice to limit the replication of the<jats:italic>virB<\/jats:italic>mutant in the spleen, suggesting that the<jats:italic>Igh6<\/jats:italic><jats:sup>\u2212<\/jats:sup><jats:sup>\/<\/jats:sup><jats:sup>\u2212<\/jats:sup>mutation affects phagocyte function and that phagocyte function can be restored by natural antibody.<\/jats:p>","DOI":"10.1128\/iai.01114-08","type":"journal-article","created":{"date-parts":[[2009,4,14]],"date-time":"2009-04-14T00:33:39Z","timestamp":1239669219000},"page":"3004-3013","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":31,"title":["Natural Antibody Contributes to Host Defense against an Attenuated<i>Brucella abortus virB<\/i>Mutant"],"prefix":"10.1128","volume":"77","author":[{"given":"Hortensia G.","family":"Rola\u0301n","sequence":"first","affiliation":[{"name":"Department of Medical Microbiology and Immunology, University of California, One Shields Avenue, Davis, California 95616"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariana N.","family":"Xavier","sequence":"additional","affiliation":[{"name":"Departamento de Cli\u0301nica e Cirurgia Veterina\u0301ria, Escola de Veterina\u0301ria, Universidade Federal de Minas Gerais, Av. Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renato L.","family":"Santos","sequence":"additional","affiliation":[{"name":"Departamento de Cli\u0301nica e Cirurgia Veterina\u0301ria, Escola de Veterina\u0301ria, Universidade Federal de Minas Gerais, Av. Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rene\u0301e M.","family":"Tsolis","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology and Immunology, University of California, One Shields Avenue, Davis, California 95616"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"207","volume":"12","year":"1999","unstructured":"Araj, G. F. 1999. Human brucellosis: a classical infectious disease with persistent diagnostic challenges. Clin. Lab. Sci.12:207-212.","journal-title":"Clin. Lab. 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