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Description of inflammation and cytokine profile at the inoculation site and in heart tissue of mice re-infected with Trypanosoma cruzi vector derived-metacyclic trypomastigotes

Published online by Cambridge University Press:  06 January 2005

L. GÓMEZ-GARCÍA
Affiliation:
Laboratorio Inmunoparasitología, Instituto Nacional Cardiología “Ignacio Chávez”, México DF
R. ALEJANDRE-AGUILAR
Affiliation:
Departamento Parasitología, Escuela Nacional Ciencias Biológicas, IPN, México DF
A. ARANDA-FRAUSTRO
Affiliation:
Laboratorio Inmunoparasitología, Instituto Nacional Cardiología “Ignacio Chávez”, México DF
R. LOPEZ
Affiliation:
Centro de Investigación en Enfermedades Tropicales, Universidad Autónoma de Campeche, México
V. M. MONTEÓN
Affiliation:
Centro de Investigación en Enfermedades Tropicales, Universidad Autónoma de Campeche, México
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Abstract

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We studied the role of Trypanosoma cruzi reinfection in regard to inflammatory and cytokine response at the inoculation site, lymph node and heart. We reinfected Balb/c mice intradermically into the hind foot-pad with natural infective metacyclic trypomastigotes. They were followed from 24 h to 30 days after the last reinfection. At the inoculation site 24 h after the last re-infection, the infiltrating inflammatory cells increased dramatically with respect to baseline inflammation, reaching maximum infiltrates for the third day. In contrast, parasite DNA was undetectable 24 h after inoculation, despite poor cytokine induction, only IFN-gamma, IL-12 and TGF-β were noticeable on days 7 and 15, whereas in the lymph nodes draining the inoculation site positive expression of IL-2, IL-4, IL-12 and TGF-beta were found to be induced as soon as 24 h after re-entry of parasite. In the heart, the inflammatory response increased immediately 24 h after re-entry of parasites, reaching its maximum on the 7th day and returning to baseline on day 30. In conclusion, although the inflammatory response is triggered in both compartments by re-entry of parasites, the inflammatory process returns almost to baseline after 30 days, leaving a persistent low-grade inflammation.

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Type
Research Article
Copyright
© 2005 Cambridge University Press