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Infection and Immunity, December 1999, p. 6631-6636, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Calgranulin C Has Filariacidal and Filariastatic Activity

John D. Gottsch,1,* Steven W. Eisinger,2 Sammy H. Liu,1 and Alan L. Scott2

Wilmer Ophthalmological Institute, School of Medicine,1 and Department of Molecular Microbiology and Immunology, School of Hygiene and Public Health,2 Johns Hopkins University, Baltimore, Maryland 21205

Received 27 May 1999/Returned for modification 5 August 1999/Accepted 10 September 1999

The calgranulins are a family of calcium- and zinc-binding proteins produced by neutrophils, monocytes, and other cells. Calgranulins are released during inflammatory responses and have antimicrobial activity. Recently, one of the calgranulins, human calgranulin C (CaGC), has been implicated as an important component of the host responses that limit the parasite burden during filarial nematode infections. The goal of this work was to test the hypothesis that human CaGC has biologic activity against filarial parasites. Brugia malayi microfilariae and adults were exposed in vitro to 0.75 to 100 nM recombinant human CaGC. Recombinant CaGC affected adult and larval parasites in a dose-dependent fashion. Microfilariae were more sensitive to the action of CaGC than were adult parasites. At high levels, CaGC was both macrofilariacidal and microfilariacidal. At lower levels, the percentage of parasites killed was dependent on the level of CaGC in the culture system. The larvae not killed had limited motility. The filariastatic effect of low-level CaGC was reversed when the CaGC was removed from the culture system. Immunohistochemical analysis demonstrated that human CaGC accumulated in the cells of the hypodermis-lateral chord of adult and larval parasites. The antifilarial activity of CaGC was not due to the sequestration of zinc. Thus, the cellular and molecular mechanisms that result in the production and release of CaGC in humans may play a key role in the regulation of filarial parasite numbers.

* Corresponding author. Mailing address: Wilmer Eye Institute, Johns Hopkins Hospital, 600 N. Wolfe Street, Baltimore, MD 21205. Phone: (410) 955-7929; Fax: (410) 614-2816. E-mail: jgottsch{at}jhmi.edu.

Infection and Immunity, December 1999, p. 6631-6636, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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