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Infection and Immunity, July 2001, p. 4342-4350, Vol. 69, No. 7
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.7.4342-4350.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Polysaccharide Biosynthesis Locus Required for Virulence of Bacteroides fragilis

Michael J. Coyne,1 Arthur O. Tzianabos,1 Benjamin C. Mallory,1 Vincent J. Carey,1 Dennis L. Kasper,1,2 and Laurie E. Comstock1,*

Channing Laboratory, Department of Medicine, Brigham and Women's Hospital,1 and Department of Microbiology and Molecular Genetics,2 Harvard Medical School, Boston, Massachusetts 02115

Received 25 January 2001/Returned for modification 10 April 2001/Accepted 19 April 2001

Bacteroides fragilis, though only a minor component of the human intestinal commensal flora, is the anaerobe most frequently isolated from intra-abdominal abscesses. B. fragilis 9343 expresses at least three capsular polysaccharides---polysaccharide A (PS A), PS B, and PS C. Purified PS A and PS B have been tested in animal models and are both able to induce the formation of intra-abdominal abscesses. Mutants unable to synthesize PS B or PS C still facilitate abscess formation at levels comparable to those of wild-type 9343. To determine the contribution of PS A to abscess formation in the context of the intact organism, the PS A biosynthesis region was cloned, sequenced, and deleted from 9343 to produce a PS A-negative mutant. Animal experiments demonstrate that the abscess-inducing capability of 9343 is severely attenuated when the organism cannot synthesize PS A, despite continued synthesis of the other capsular polysaccharides. The PS A of 9343 contains an unusual free amino sugar that is essential for abscess formation by this polymer. PCR analysis of the PS A biosynthesis loci of 50 B. fragilis isolates indicates that regions flanking each side of this locus are conserved in all strains. The downstream conserved region includes two terminal PS A biosynthesis genes that homology-based analyses predict are involved in the synthesis and transfer of the free amino sugar of PS A. Conservation of these genes suggests that this sugar is present in the PS A of all serotypes and may explain the abscessogenic nature of B. fragilis.

* Corresponding author. Mailing address: Channing Laboratory, 181 Longwood Ave., Boston, MA 02115. Phone: (617) 525-2679. Fax: (617) 731-1541. E-mail: lcomstock{at}channing.harvard.edu.

Infection and Immunity, July 2001, p. 4342-4350, Vol. 69, No. 7
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.7.4342-4350.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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