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Infection and Immunity, November 2005, p. 7442-7449, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7442-7449.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Loss of Complement Activation and Leukocyte Adherence as Nippostrongylus brasiliensis Develops within the Murine Host

Paul R. Giacomin,¹ Hui Wang,¹ David L. Gordon,² Marina Botto,³ and Lindsay A. Dent^1*

School of Molecular and Biomedical Science, University of Adelaide, Adelaide, Australia,¹ Department of Microbiology and Infectious Diseases, Flinders Medical Centre, Adelaide, Australia,² Rheumatology Section, Imperial College, Hammersmith Campus, London, United Kingdom³

Received 19 April 2005/ Returned for modification 27 May 2005/ Accepted 10 August 2005

Complement activation and C3 deposition on the surface of parasitic helminths may be important for recruitment of leukocytes and for damage to the target organism via cell-mediated mechanisms. Inhibition of complement activation would therefore be advantageous to parasites, minimizing damage and enhancing migration through tissues. The aim of this study was to determine ex vivo if complement activation by, and leukocyte adherence to, the nematode Nippostrongylus brasiliensis change as the parasite matures and migrates through the murine host. Pathways of activation of complement and the mechanism of adherence of leukocytes were also defined using sera from mice genetically deficient in either C1q, factor B, C1q and factor B, C3, or C4. Substantive deposition of C3 and adherence of eosinophil-rich leukocytes were seen with infective-stage (L3) but not with lung-stage (L4) larvae. Adult intestinal worms had low to intermediate levels of both C3 and leukocyte binding. For L3 and adult worms, complement deposition was principally dependent on the alternative pathway. For lung-stage larvae, the small amount of C3 detected was dependent to similar degrees on both the lectin and alternative pathways. The classical pathway was not involved for any of the life stages of the parasite. These results suggest that in primary infections, the infective stage of N. brasiliensis is vulnerable to complement-dependent attack by leukocytes. However, within the first 24 h of infection, N. brasiliensis acquires the ability to largely avoid complement-dependent immune responses.

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* Corresponding author. Mailing address: School of Molecular and Biomedical Science, University of Adelaide, North Terrace, Adelaide, South Australia, Australia 5005. Phone: 61 8 8303 4155. Fax: 61 8 8303 7532. E-mail: lindsay.dent{at}adelaide.edu.au.

Editor: J. F. Urban, Jr.

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Infection and Immunity, November 2005, p. 7442-7449, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7442-7449.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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