This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Haapasalo, K.
Right arrow Articles by Jokiranta, T. S.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Haapasalo, K.
Right arrow Articles by Jokiranta, T. S.

 Previous Article  |  Next Article 

Infection and Immunity, September 2009, p. 3886-3893, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.01583-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Loa loa Microfilariae Evade Complement Attack In Vivo by Acquiring Regulatory Proteins from Host Plasma {triangledown}

Karita Haapasalo, Taru Meri, and T. Sakari Jokiranta*

Department of Bacteriology and Immunology, Haartman Institute and HUSLAB, University and University Central Hospital of Helsinki, Finland

Received 31 December 2008/ Returned for modification 17 February 2009/ Accepted 10 June 2009

Loa loa is a filarial nematode that infects humans. The adults live in subcutaneous tissues and produce microfilariae that live for several weeks in the blood circulation in order to be transmitted to another person via blood meals of a dipterian vector. As microfilariae live in continuous contact with plasma, it is obvious that they evade the complement system. We studied markers of complement activation and signs of complement regulation on Loa loa microfilariae in vivo. The microfilariae were isolated from anticoagulated blood samples of a Loa loa-infected Caucasian patient. C1q and some mannose-binding lectin but only a limited amount of C3b or C4b fragments and practically no C5 or C5b-9 were present on the microfilariae. The covalently microfilaria-bound C3 and C4 depositions were mainly inactive iC3b, C3c, and iC4b fragments indicating that microfilariae had regulated complement activation in vivo. Also, in vitro deposition of C3b onto the microfilariae upon serum exposure was limited. The patient-isolated microfilariae were found to carry the host complement regulators factor H and C4b-binding protein on the outermost layer, so called sheath. The microfilaria-bound factor H was functionally active. Binding of the complement regulators to the microfilariae was confirmed in vitro using 125I-labeled factor H and C4b-binding protein. In conclusion, our study shows that Loa loa microfilariae block complement activation and acquire the host complement regulators factor H and C4b-binding protein in blood circulation. This is the first time that binding of complement regulators onto nonviral pathogens has been demonstrated to occur in humans in vivo.

* Corresponding author. Mailing address: Haartman Institute, Department of Bacteriology and Immunology, P.O. Box 21, FIN-00014 University of Helsinki, Finland. Phone: 358-9-1911. Fax: 358-9-1912 6382. E-mail: sakari.jokiranta{at}helsinki.fi

{triangledown} Published ahead of print on 15 June 2009.

Editor: J. F. Urban, Jr.

Infection and Immunity, September 2009, p. 3886-3893, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.01583-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»