{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T16:45:01Z","timestamp":1790873101304,"version":"4.1.0"},"reference-count":45,"publisher":"American Society for Microbiology","issue":"18","license":[{"start":{"date-parts":[[2008,9,15]],"date-time":"2008-09-15T00:00:00Z","timestamp":1221436800000},"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":["J Bacteriol"],"published-print":{"date-parts":[[2008,9,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Brucella<\/jats:italic>\n            genomic islands (GIs) share similarities in their genomic organization to pathogenicity islands from other bacteria and are likely acquired by lateral gene transfer. Here, we report the identification of a GI that is important for the pathogenicity of\n            <jats:italic>Brucella melitensis<\/jats:italic>\n            . The deletion of GI-1, GI-5, or GI-6 did not affect bacterial growth in macrophages as well as their virulence in interferon regulatory factor 1-deficient (IRF-1\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ) mice, suggesting that these islands do not contribute to\n            <jats:italic>Brucella<\/jats:italic>\n            virulence. However, the deletion of GI-2 resulted in the attenuation of bacterial growth in macrophages and virulence in IRF-1\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. The GI-2 mutant also displayed a rough lipopolysaccharide (LPS) phenotype indicated by acriflavin agglutination, suggesting that in vitro and in vivo attenuation is a result of LPS alteration. Further, systematic analysis of the entire GI-2 revealed two open reading frames (ORFs), BMEI0997 and I0998, that encode hypothetical sugar transferases and contribute to LPS alteration, as the deletion of either of these ORFs resulted in a rough phenotype similar to that of the GI-2 mutant. Complementation analyses indicated that in addition to I0997 and I0998, I0999 is required to restore the smooth LPS in the GI-2 mutant as well as its full in vitro and in vivo virulence. The I0999 sequence analysis suggested that it might function as a transporter to help facilitate the transport or linking of the O antigen to the LPS. Our study also indicated that the rough LPS resulting from the GI-2 deletion may affect pathogen-associated molecular pattern recognition by Toll-like receptors.\n          <\/jats:p>","DOI":"10.1128\/jb.00520-08","type":"journal-article","created":{"date-parts":[[2008,7,19]],"date-time":"2008-07-19T00:54:50Z","timestamp":1216428890000},"page":"6243-6252","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":31,"title":["Genomic Island 2 of\n            <i>Brucella melitensis<\/i>\n            Is a Major Virulence Determinant: Functional Analyses of Genomic Islands"],"prefix":"10.1128","volume":"190","author":[{"given":"Gireesh","family":"Rajashekara","sequence":"first","affiliation":[{"name":"Food Animal Health Research Program, Ohio Agricultural Research Development Center, Department of Veterinary Preventive Medicine, The Ohio State University, Wooster, Ohio 44691"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jill","family":"Covert","sequence":"additional","affiliation":[{"name":"Department of Animal Health and Biomedical Sciences, University of Wisconsin, 1656 Linden Drive, Madison, Wisconsin 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"Petersen","sequence":"additional","affiliation":[{"name":"Department of Animal Health and Biomedical Sciences, University of Wisconsin, 1656 Linden Drive, Madison, Wisconsin 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda","family":"Eskra","sequence":"additional","affiliation":[{"name":"Department of Animal Health and Biomedical Sciences, University of Wisconsin, 1656 Linden Drive, Madison, Wisconsin 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gary","family":"Splitter","sequence":"additional","affiliation":[{"name":"Department of Animal Health and Biomedical Sciences, University of Wisconsin, 1656 Linden Drive, Madison, Wisconsin 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"499","DOI":"10.1038\/nri1391","volume":"4","year":"2004","unstructured":"Akira, S., and K. 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