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Capsule synthesis by Bacillus anthracis is required for dissemination in murine inhalation anthrax
Author(s) -
Drysdale Melissa,
Heninger Sara,
Hutt Julie,
Chen Yahua,
Lyons C Rick,
Koehler Theresa M
Publication year - 2005
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7600495
Subject(s) - bacillus anthracis , biology , microbiology and biotechnology , anthrax vaccines , anthrax toxin , bacillus (shape) , bacillus subtilis , bacteria , virology , immunology , immunization , genetics , antigen , gene , fusion protein , recombinant dna , dna vaccination
Bacillus anthracis , the agent of anthrax, produces a poly‐ D ‐glutamic acid capsule that has been implicated in virulence. Many strains missing pXO2 (96 kb), which harbors the capsule biosynthetic operon capBCAD , but carrying pXO1 (182 kb) that harbors the anthrax toxin genes, are attenuated in animal models. Also, noncapsulated strains are readily phagocytosed by macrophage cell lines, whereas capsulated strains are resistant to phagocytosis. We show that a strain carrying both virulence plasmids but deleted specifically for capBCAD is highly attenuated in a mouse model for inhalation anthrax. The parent strain and capsule mutant initiated germination in the lungs, but the capsule mutant did not disseminate to the spleen. A mutant harboring capBCAD but deleted for the cap regulators acpA and acpB was also significantly attenuated, in agreement with the capsule‐negative phenotype during in vitro growth. Surprisingly, an acpB mutant, but not an acpA mutant, displayed an elevated LD 50 and reduced ability to disseminate, indicating that acpA and acpB are not true functional homologs and that acpB may play a larger role in virulence than originally suspected.