Open Access Highly Accessed Research article

In vivo involvement of polymorphonuclear neutrophils in Leishmania infantum infection

Déborah Rousseau1, Sylvie Demartino1, Bernard Ferrua1, Jean François Michiels2, Fabienne Anjuère1, Konstantina Fragaki1, Yves Le Fichoux12 and Joanna Kubar1*

Author Affiliations

1 Groupe de Recherche en Immunopathologie de la Leishmaniose (EA 2675),INSERM U364, IFR 50, Faculté de Médecine, 06107 Nice Cedex 2, France

2 Laboratoire de Parasitologie Hôpital de l'Archet, Nice Cedex 3, France

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BMC Microbiology 2001, 1:17  doi:10.1186/1471-2180-1-17

Published: 17 August 2001



The role of lymphocytes in the specific defence against L. infantum has been well established, but the part played by polynuclear neutrophil (PN) cells in controlling visceral leishmaniasis was much less studied. In this report we examine in vivo the participation of PN in early and late phases of infection by L. infantum.


Promastigote phagocytosis and killing occurs very early after infection, as demonstrated by electron microscopy analyses which show in BALB/c mouse spleen, but not in liver, numerous PN harbouring ultrastructurally degraded parasites. It is shown, using mAb RB6-8C5 directed against mature mouse granulocytes, that in chronically infected mice, long-term PN depletion did not enhance parasite counts neither in liver nor in spleen, indicating that these cells are not involved in the late phase of L. infantum infection. In acute stage of infection, in mouse liver, where L. infantum load is initially larger than that in spleen but resolves spontaneously, there was no significant effect of neutrophils depletion. By contrast, early in infection the neutrophil cells crucially contributed to parasite killing in spleen, since PN depletion, performed before and up to 7 days after the parasite inoculation, resulted in a ten-fold increase of parasite burden.


Taken together these data show that neutrophil cells contribute to the early control of the parasite growth in spleen but not in liver and that these cells have no significant effect late in infection in either of these target organs.