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Journal of Bacteriology, September 2008, p. 6243-6252, Vol. 190, No. 18
0021-9193/08/$08.00+0     doi:10.1128/JB.00520-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Genomic Island 2 of Brucella melitensis Is a Major Virulence Determinant: Functional Analyses of Genomic Islands{triangledown} ,{dagger}

Gireesh Rajashekara,1* Jill Covert,2 Erik Petersen,2 Linda Eskra,2 and Gary Splitter2*

Food Animal Health Research Program, Ohio Agricultural Research Development Center, Department of Veterinary Preventive Medicine, The Ohio State University, Wooster, Ohio 44691,1 Department of Animal Health and Biomedical Sciences, University of Wisconsin, 1656 Linden Drive, Madison, Wisconsin 537062

Received 16 April 2008/ Accepted 6 July 2008

Brucella 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 Brucella melitensis. 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–/–) mice, suggesting that these islands do not contribute to Brucella virulence. However, the deletion of GI-2 resulted in the attenuation of bacterial growth in macrophages and virulence in IRF-1–/– 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.

* Corresponding author. Mailing address for Gireesh Rajashekara: Food Animal Health Research Program, Ohio Agricultural Research Development Center, Department of Veterinary Preventive Medicine, The Ohio State University, Wooster, OH 44691. Phone: (330) 263-3745. Fax: (330) 263-3677. E-mail: rajashekara.2{at}osu.edu. Mailing address for Gary A. Splitter: Department of Animal Health and Biomedical Sciences, University of Wisconsin, 1656 Linden Drive, Madison, WI 53706. Phone: (608) 262-1837. Fax: (608) 262-7420. E-mail: splitter{at}svm.vetmed.wisc.edu

{triangledown} Published ahead of print on 18 July 2008.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

Journal of Bacteriology, September 2008, p. 6243-6252, Vol. 190, No. 18
0021-9193/08/$08.00+0     doi:10.1128/JB.00520-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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