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Leishmania infantum: soluble proteins released by the parasite exert differential effects on host immune response

R Rosa1, O Roos Rodrigues, C Marques

  • 1Unidade de Leishmanioses e Centro de Malária e Outras Doenças Tropicais, Instituto de Higiene e Medicina Tropical (IHMT), Universidade Nova de Lisboa, Rua da Junqueira 96, 1349-008 Lisboa, Portugal.

Experimental Parasitology
|February 3, 2005
PubMed

Insights

Leishmania infantum proteins modulate host immunity differently in BALB/c and C57BL/6 mice. Protein fractions impact cytokine production (IL-4, IL-12), influencing parasite control based on host genetics and infection stage.

Area of Science:

  • Immunology
  • Parasitology
  • Molecular Biology

Background:

  • Leishmania infantum causes visceral leishmaniasis.
  • Host immune response and genetic background influence disease outcome.
  • Parasite-derived proteins may modulate host immunity.

Purpose of the Study:

  • To analyze the modulatory effect of Leishmania infantum promastigote-released proteins on the cellular immune response.
  • To investigate these effects in susceptible (BALB/c) and resistant (C57BL/6) mouse strains at different infection time points (30 and 45 days).

Main Methods:

  • Cultured Leishmania infantum promastigotes released protein fractions (High, Inter, Low).
  • Spleen cells from infected BALB/c and C57BL/6 mice were stimulated with these fractions.
  • Cell proliferation and cytokine expression (IL-4, IL-12) were analyzed.

Main Results:

  • In C57BL/6 mice, protein fractions stimulated spleen cell proliferation and cytokine expression.
  • In C57BL/6 mice, the Low protein fraction induced IL-4 release following parasite load decrease.
  • In BALB/c mice, specific immune responses were observed at higher parasitic loads, with Inter fraction promoting IL-4 and High/Low fractions inducing IL-12.

Conclusions:

  • Leishmania infantum protein fractions play a role in modulating host immunity.
  • The immune modulation depends on host genetic background and parasite load.
  • These proteins are critical in controlling parasite replication and preventing premature host death.

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