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Infection and Immunity, November 2004, p. 6642-6649, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6642-6649.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Mast Cell-Dependent Control of Giardia lamblia Infections in Mice

Erqiu Li, Ping Zhou, Ziva Petrin,{dagger} and Steven M. Singer*

Department of Biology, Georgetown University, Washington, D.C.

Received 5 April 2004/ Returned for modification 22 May 2004/ Accepted 3 August 2004

Mast cells are important for protective immunity to intestinal helminth infections and as mediators of allergic disease. Their role in protozoan infections is less well described. We have therefore analyzed mast cell responses and parasite control in mice infected with the protozoan Giardia lamblia. We also measured immunoglobulin A (IgA) responses to the parasite, as IgA can have a protective role in this model. c-kitw/wv mice failed to make parasite-specific IgA, mount a mast cell response, or eliminate the infection. Anti-c-kit-treated C57BL/6 mice had normal IgA responses, lacked mast cell responses, had reduced interleukin-6 (IL-6) mRNA in the small intestine, and failed to control the infection within 10 days. IL-9-deficient mice had a significant but reduced mast cell response and still controlled the infection within 2 weeks. Interestingly, IL-6-deficient mice had enhanced mast cell responses yet failed to rapidly control the infection. However, prevention of mast cell responses in IL-6-deficient mice by anti-c-kit treatment did not lead to parasite elimination. Both IL-6- and IL-9-deficient mice had normal IgA production. IL-6-deficient mice had significant serum levels of mast cell mediators, histamine and mast cell protease 1, following infection. Together, these results show that mast cells are important for the rapid control of Giardia infections in mice. Furthermore, they show that IL-6 is not necessary for these mast cell responses. Instead, they suggest that mast cell production of IL-6 appears to be important for control of this infection.

* Corresponding author. Mailing address: Department of Biology, Reiss 406, Georgetown University, Washington, DC 20057. Phone: (202) 687-9884. Fax: (202) 687-5662. E-mail: sms3{at}georgetown.edu.

Editor: W. A. Petri, Jr.

{dagger} Present address: University of Ljubljana Medical School, 1104 Ljubljana, Slovenia.

Infection and Immunity, November 2004, p. 6642-6649, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6642-6649.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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