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Infect. Immun. doi:10.1128/IAI.00434-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Bacillus anthracis Spores of the bclA Mutant Exhibit Increased Adherence to Epithelial, Fibroblast, and Endothelial Cells but not Macrophages

Bacteriology Division, Integrated Toxicology Division, and Headquarters, U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, Frederick, Maryland

^* To whom correspondence should be addressed. Email: joel.a.bozue{at}us.army.mil.

	Abstract

Bacillus anthracis is the causative agent of anthrax, and the spore form of the bacterium represents the infectious particle introduced into a host. The spore is surrounded by an exosporium, a loose-fitting membrane composed of proteins and carbohydrates from which hair-like projections extend. These projections are composed mainly of the BclA (Bacillus-collagen-like) protein. To date, exact roles of the exosporium structure and BclA protein remain undetermined. We examined differences in spore binding of wild-type Ames and a bclA mutant of B. anthracis to bronchial epithelial cells, as well as to other epithelial cells: A549, CHO, and Caco-2; IMR-90, a fibroblast cell line; and human umbilical vein vascular endothelium cells. Binding of wild-type Ames spores to bronchial epithelial cells appeared to be a dose-dependent, receptor-ligand mediated event. There were similar findings for the bclA mutant, with an additional non-specific binding component likely leading to significantly more adherence to all non-professional phagocytic cell types. In contrast, we detected no difference in adherence and uptake of spores by macrophages for either wild-type Ames or the bclA mutant strain. These results suggest that one potential role of the BclA fibers may be to inhibit non-specific interactions between B. anthracis spores with non-professional phagocytic cells and thus direct the spores towards uptake by macrophages during initiation of infection in mammals.

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