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Infection and Immunity, June 2006, p. 3170-3179, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.01648-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Macrophage Migration Inhibitory Factor Contributes to Host Defense against Acute Trypanosoma cruzi Infection

José L. Reyes,1 Luis I. Terrazas,1 Bertha Espinoza,2 David Cruz-Robles,3 Virgilia Soto,3 Irma Rivera-Montoya,1 Lorena Gómez-García,1,3 Heidi Snider,4 Abhay R. Satoskar,4 and Miriam Rodríguez-Sosa1*

Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de México (UNAM) Tlalnepantla,1 Instituto de Investigaciones Biomédicas, UNAM,2 Instituto Nacional de Cardiología Ignacio Chávez, Mexico D.F., México,3 Department of Microbiology, The Ohio State University, Columbus, Ohio4

Received 7 October 2005/ Returned for modification 12 December 2005/ Accepted 15 March 2006

Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that is involved in the host defense against several pathogens. Here we used MIF–/– mice to determine the role of endogenous MIF in the regulation of the host immune response against Trypanosoma cruzi infection. MIF–/– mice displayed high levels of blood and tissue parasitemia, developed severe heart and skeletal muscle immunopathology, and succumbed to T. cruzi infection faster than MIF+/+ mice. The enhanced susceptibility of MIF–/– mice to T. cruzi was associated with reduced levels of proinflammatory cytokines, such as tumor necrosis factor alpha, interleukin-12 (IL-12), IL-18, gamma interferon (IFN-{gamma}), and IL-1ß, in their sera and reduced production of IL-12, IFN-{gamma}, and IL-4 by spleen cells during the early phase of infection. At all time points, antigen-stimulated splenocytes from MIF+/+ and MIF–/– mice produced comparable levels of IL-10. MIF–/– mice also produced significantly less Th1-associated antigen-specific immunoglobulin G2a (IgG2a) throughout the infection, but both groups produced comparable levels of Th2-associated IgG1. Lastly, inflamed hearts from T. cruzi-infected MIF–/– mice expressed increased transcripts for IFN-{gamma}, but fewer for IL-12 p35, IL-12 p40, IL-23, and inducible nitric oxide synthase, compared to MIF+/+ mice. Taken together, our findings show that MIF plays a role in controlling acute T. cruzi infection.

* Corresponding author. Mailing address: Unidad de Biomedicina, FES-Iztacala, UNAM, Av. De los Barrios #1, Los Reyes Iztacala, 54090 Tlalnepantla, Edo. de México, Mexico. Phone: (5255) 5623-1291, ext. 438. Fax: (5255) 5623-1225. E-mail: rodriguezm{at}campus.iztacala.unam.mx.

Editor: J. F. Urban, Jr.

Infection and Immunity, June 2006, p. 3170-3179, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.01648-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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