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Infection and Immunity, October 2004, p. 5676-5686, Vol. 72, No. 10
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.10.5676-5686.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The Glycan-Rich Outer Layer of the Cell Wall of Mycobacterium tuberculosis Acts as an Antiphagocytic Capsule Limiting the Association of the Bacterium with Macrophages

Richard W. Stokes,1,2,3,4,5* Raymond Norris-Jones,2 Donald E. Brooks,2 Terry J. Beveridge,5,6 Dan Doxsee,1 and Lisa M. Thorson1

Departments of Paediatrics,1 Pathology & Laboratory Medicine,2 Microbiology & Immunology, University of British Columbia,3 Division of Infectious and Immunological Diseases, British Columbia's Children's Hospital,4 Canadian Bacterial Diseases Network National Centres of Excellence, Vancouver, British Columbia,5 Department of Microbiology, College of Biological Science, University of Guelph, Guelph, Ontario, Canada6

Received 23 January 2004/ Returned for modification 14 April 2004/ Accepted 20 July 2004

Mycobacterium tuberculosis, the causative agent of tuberculosis, is a facultative intracellular pathogen that infects macrophages and other host cells. We show that sonication of M. tuberculosis results in the removal of material from the surface capsule-like layer of the bacteria, resulting in an enhanced propensity of the bacteria to bind to macrophages. This effect is observed with disparate murine and human macrophage populations though, interestingly, not with freshly explanted alveolar macrophages. Enhanced binding to macrophages following sonication is significantly greater within members of the M. tuberculosis family (pathogens) than within the Mycobacterium avium complex (opportunistic pathogens) or for Mycobacterium smegmatis (saprophyte). Sonication does not affect the viability or the surface hydrophobicity of M. tuberculosis but does result in changes in surface charge and in the binding of mannose-specific lectins to the bacterial surface. The increased binding of sonicated M. tuberculosis was not mediated through complement receptor 3. These results provide evidence that the surface capsule on members of the M. tuberculosis family may be an important virulence factor involved in the survival of M. tuberculosis in the mammalian host. They also question the view that M. tuberculosis is readily ingested by any macrophage it encounters and support the contention that M. tuberculosis, like many other microbial pathogens, has an antiphagocytic capsule that limits and controls the interaction of the bacterium with macrophages.

* Corresponding author. Mailing address: Department of Paediatrics, The Research Institute, 950 West 28th Ave., Vancouver, British Columbia, V5Z 4H4 Canada. Phone: (604) 875 2466. Fax: (604) 875 2226. E-mail: rstokes{at}cbdn.ca.

Editor: J. D. Clements

Infection and Immunity, October 2004, p. 5676-5686, Vol. 72, No. 10
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.10.5676-5686.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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