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Infection and Immunity, March 2003, p. 1247-1254, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1247-1254.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Macrophage Migration Inhibitory Factor Plays a Critical Role in Mediating Protection against the Helminth Parasite Taenia crassiceps

Miriam Rodríguez-Sosa,1 Lucia E. Rosas,2 John R. David,3 Rafael Bojalil,1 Abhay R. Satoskar,2* and Luis I. Terrazas1*

Department of Immunology, Instituto Nacional de Cardiología "Ignacio Chávez," Mexico, D.F. 14080 Mexico,1 Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115,3 Department of Microbiology, The Ohio State University, Columbus, Ohio 432102

Received 19 August 2002/ Returned for modification 12 November 2002/ Accepted 13 December 2002

To determine the role of endogenous migration inhibitory factor (MIF) in regulation of immune response during murine cysticercosis caused by the helminth parasite Taenia crassiceps, we analyzed the course of T. crassiceps infection in MIF-/- BALB/c mice. MIF-/- mice were highly susceptible to T. crassiceps and developed significantly higher parasite loads compared to similarly infected MIF+/+ mice. Throughout the course of infection, Taenia crassiceps soluble antigen-stimulated spleen cells from both MIF+/+ and MIF-/- mice produced significant and comparable levels of interleukin-4 (IL-4), but those from MIF-/- mice produced significantly more IL-13, as well as gamma interferon (IFN-{gamma}), suggesting that the susceptibility of MIF-/- mice to T. crassiceps was not due to the lack of IFN-{gamma} production. Interestingly, low levels of both total and specific immunoglobulin G2a were observed in MIF-/- cysticercotic mice despite the high IFN-{gamma} levels; in addition, peritoneal macrophages obtained from T. crassiceps-infected MIF-/- mice at different time points failed to respond efficiently to stimulation in vitro with lipopolysaccharide plus IFN-{gamma} and produced significantly lower levels of IL-12, tumor necrosis factor alpha, and NO compared to those from MIF+/+ mice. These findings demonstrate that MIF plays a critical role in mediating protection against T. crassiceps in vivo. Moreover, these findings also suggest that impaired macrophage function rather than the lack of Th1 development may be responsible for mediating susceptibility to T. crassiceps.

* Corresponding author. Mailing address: Department of Microbiology, The Ohio State University, Columbus, OH 43210. Phone: (614) 292-3243. Fax: (614) 292-8120. E-mail: satoskar.2{at}osu.edu.

* Corresponding author. Mailing address: Department of Immunology, Instituto Nacional de Cardiología "Ignacio Chávez," México, D.F. 14080 México. Phone: (5255) 5573-2911. Fax: (5255) 5573-0994. E-mail: terlui{at}cardiologia.org.mx.

Editor: J. M. Mansfield

Infection and Immunity, March 2003, p. 1247-1254, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1247-1254.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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