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Infection and Immunity, December 2001, p. 7729-7735, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7729-7735.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Role of Complement in Mycobacterium avium Pathogenesis: In Vivo and In Vitro Analyses of the Host Response to Infection in the Absence of Complement Component C3

Suzanne S. Bohlson, Jennifer A. Strasser, Jacquelyn J. Bower, and Jeffrey S. Schorey*

Department of Biology, University of Notre Dame, Notre Dame, Indiana 46617

Received 23 March 2001/Returned for modification 2 May 2001/Accepted 6 September 2001

We investigated the importance of the host complement system in the pathogenesis of disease mediated by the intramacrophage pathogen Mycobacterium avium. Mycobacteria opsonized with complement are efficiently ingested by macrophages through various complement receptors. Furthermore, unlike other bacteria, mycobacteria can activate both the alternative and classical complement pathways in the absence of specific antibodies. Therefore, to examine the role of complement in the mycobacterial infection process in vivo, mice deficient in complement component C3 were infected with M. avium. Surprisingly, C3-deficient mice infected intravenously with M. avium displayed no difference in bacterial burden or granulomatous response compared to wild-type control mice. C3-sufficient mice and C3-deficient mice were equally susceptible to infection by M. avium regardless of the genotype at the bcg locus, a locus known to confer susceptibility to infection with intracellular pathogens. In vitro studies using mouse bone marrow-derived macrophages resulted in significant M. avium invasion of macrophages in the absence of C3; however, the kinetics of infection were delayed compared to complement-mediated invasion. The data indicate that complement does not play an essential role in mediating M. avium infections in the mouse and suggest either that other invasion mechanisms can compensate for the absence of complement-mediated entry or that complement is not a major mycobacterial opsonin in vivo.

* Corresponding author. Mailing address: Department of Biology, University of Notre Dame, 130 Galvin Life Science Center, Notre Dame, IN 46656. Phone: (219) 631-3734. Fax: (219) 631-7413. E-mail: Schorey.1{at}nd.edu.

Infection and Immunity, December 2001, p. 7729-7735, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7729-7735.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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