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Mediators of Inflammation
Volume 2014 (2014), Article ID 506450, 12 pages
http://dx.doi.org/10.1155/2014/506450
Research Article

TRPV1 Antagonism by Capsazepine Modulates Innate Immune Response in Mice Infected with Plasmodium berghei ANKA

1Universidade CEUMA, 65075-120 São Luís, MA, Brazil
2Cardiovascular Division, King’s College London, London, UK
3Universidade de São Paulo, São Paulo, Brazil
4Universidade Federal de São Paulo, Diadema, Brazil
5Universidade Federal do Maranhão, São Luís, Brazil
6Instituto Florence de Ensino Superior, São Luís, Brazil

Received 3 June 2014; Accepted 8 July 2014; Published 24 August 2014

Academic Editor: Mauricio Martins Rodrigues

Copyright © 2014 Elizabeth S. Fernandes et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Thousands of people suffer from severe malaria every year. The innate immune response plays a determinant role in host’s defence to malaria. Transient receptor potential vanilloid 1 (TRPV1) modulates macrophage-mediated responses in sepsis, but its role in other pathogenic diseases has never been addressed. We investigated the effects of capsazepine, a TRPV1 antagonist, in malaria. C57BL/6 mice received 105 red blood cells infected with Plasmodium berghei ANKA intraperitoneally. Noninfected mice were used as controls. Capsazepine or vehicle was given intraperitoneally for 6 days. Mice were culled on day 7 after infection and blood and spleen cell phenotype and activation were evaluated. Capsazepine decreased circulating but not spleen F4/80+Ly6G+ cell numbers as well as activation of both F4/80+and F4/80+Ly6G+ cells in infected animals. In addition, capsazepine increased circulating but not spleen GR1+ and natural killer (NK) population, without interfering with natural killer T (NKT) cell numbers and blood NK and NKT activation. However, capsazepine diminished CD69 expression in spleen NKT but not NK cells. Infection increased lipid peroxidation and the release of TNFα and IFNγ, although capsazepine-treated group exhibited lower levels of lipid peroxidation and TNFα. Capsazepine treatment did not affect parasitaemia. Overall, TRPV1 antagonism modulates the innate immune response to malaria.