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Infection and Immunity, September 2009, p. 3679-3685, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00233-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Complement C3 Plays an Essential Role in the Control of Opportunistic Fungal Infections{triangledown}

S. Vicky Tsoni,1 Ann M. Kerrigan,1 Mohlopheni J. Marakalala,1 Naren Srinivasan,1 Maureen Duffield,2 Philip R. Taylor,3 Marina Botto,4 Chad Steele,5 and Gordon D. Brown1,6*

Institute of Infectious Disease and Molecular Medicine, Division of Immunology,1 Department of Anatomical Pathology, CLS, University of Cape Town, Cape Town 7925, South Africa,2 Department of Medical Biochemistry and Immunology, Cardiff University School of Medicine, Cardiff CF14 4XN, United Kingdom,3 Imperial College, Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom,4 Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama,5 Aberdeen Fungal Group, Section of Immunology and Infection, Division of Applied Medicine, Institute of Medical Sciences, Foresterhill, University of Aberdeen, Aberdeen AB25 2ZD, United Kingdom6

Received 27 February 2009/ Returned for modification 12 April 2009/ Accepted 23 May 2009

The innate recognition of fungal pathogens is a crucial first step in the induction of protective antifungal immunity. Complement is thought to be one key component in this process, facilitating fungal recognition and inducing early inflammation. However, the roles of the individual complement components have not been examined extensively. Here we have used mice lacking C3 to examine its role in immunity to opportunistic fungal pathogens and show that this complement component is essential for resistance to infections with Candida albicans and Candida glabrata. We demonstrate that the absence of C3 impairs fungal clearance but does not affect inflammatory responses. We also show that the presence of C3 contributes to mortality in mice challenged with very high doses of Saccharomyces cerevisiae, although these effects were found to be mouse strain dependent.

* Corresponding author. Mailing address: Section of Immunity and Infection, Room 4.20, Institute of medical sciences, University of Aberdeen, Ashgrove Road West, Aberdeen, United Kingdom AB25 2ZD. Phone: 44-1224-555796. Fax: 44-1224-555844. E-mail: gordon.brown{at}abdn.ac.uk

{triangledown} Published ahead of print on 6 July 2009.

Editor: A. Casadevall

Infection and Immunity, September 2009, p. 3679-3685, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00233-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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