Parasites & Vectors (Nov 2012)

Resistance to visceral leishmaniasis is severely compromised in mice deficient of bradykinin B2-receptors

  • Nico Dirlei,
  • Feijó Daniel,
  • Maran Naiara,
  • Morrot Alexandre,
  • Scharfstein Julio,
  • Palatnik Marcos,
  • Palatnik-de-Sousa Clarisa

DOI
https://doi.org/10.1186/1756-3305-5-261
Journal volume & issue
Vol. 5, no. 1
p. 261

Abstract

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Abstract Background Kinins liberated from plasma–borne kininogens, are potent innate stimulatory signals. We evaluated whether resistance to infection by Leishmania (L.) chagasi depends on activation of G-protein coupled bradykinin B2 receptors (B2R). Findings B2R −/− C57BL/6 knock-out (KOB2) and B2R+/+ C57BL/6-wild type control mice (C57) were infected with amastigotes of Leishmania (L.) chagasi. Thirty days after infection, the KOB2 mice showed 14% and 32% relative increases of liver (p Conclusions We found that mice lacking B2R display increased susceptibility to the infection by Leishmania (L.) chagasi. Our findings suggest that activation of the bradykinin/B2R pathway contributes to development of host resistance to visceral leishmaniasis.

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