Limits...
In vivo involvement of polymorphonuclear neutrophils in Leishmania infantum infection.

Rousseau D, Demartino S, Ferrua B, Michiels JF, Anjuère F, Fragaki K, Le Fichoux Y, Kubar J - BMC Microbiol. (2001)

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Groupe de Recherche en Immunopathologie de la Leishmaniose (EA 2675),INSERM U364, IFR 50, Faculté de Médecine, 06107 Nice Cedex 2, France. droussea@unice.fr

ABSTRACT

Background: 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.

Results: 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.

Conclusions: 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.

Show MeSH

Related in: MedlinePlus

Neutrophil influx to the infected spleen, shown by electron microscopy. Micrograph of spleen, 24 h after L. infantum inoculation (magnification × 1200)
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC57739&req=5

Figure 3: Neutrophil influx to the infected spleen, shown by electron microscopy. Micrograph of spleen, 24 h after L. infantum inoculation (magnification × 1200)

Mentions: In order to study the early in vivo participation of PN in host defence, spleen and liver of mice were examined by electron microscopy 1 h, 2 h, 5 h and 24 h hours after L. infantum inoculation. In liver, the parasites were readily observed already at 1 h and 2 h after the infection. All parasites were localised close to or inside macrophages and no Leishmania were detected inside neutrophil cells, at any time of observation. In contrast, in spleen tissue, parasites were much less abundant and several fields had to be screened in order to find Leishmania. A part of spleen neutrophils was found to contain at least one parasite in a more or less degraded state. Figure 2 shows that within one hour post infection, the intraneutrophil protozoan, although recognised by parietal tubules, flagellar pocket and longitudinal-cut flagella, generally lost its ultrastructural integrity. The electron microscopy images do not at all instances allow determining the precise intracellular parasite localisation, so a quantitative evaluation in spleen of the percentage of parasitised macrophages versus parasitised neutrophils would be non-reliable. Twenty-four hours after the infection, neutrophil influx was still observed in the spleen (Figure 3) but no intraneutrophil parasites were detected. In the parasitised monocytes (Figure 4) Leishmania appeared relatively intact as compared to that phagocytised by PMN.


In vivo involvement of polymorphonuclear neutrophils in Leishmania infantum infection.

Rousseau D, Demartino S, Ferrua B, Michiels JF, Anjuère F, Fragaki K, Le Fichoux Y, Kubar J - BMC Microbiol. (2001)

Neutrophil influx to the infected spleen, shown by electron microscopy. Micrograph of spleen, 24 h after L. infantum inoculation (magnification × 1200)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC57739&req=5

Figure 3: Neutrophil influx to the infected spleen, shown by electron microscopy. Micrograph of spleen, 24 h after L. infantum inoculation (magnification × 1200)
Mentions: In order to study the early in vivo participation of PN in host defence, spleen and liver of mice were examined by electron microscopy 1 h, 2 h, 5 h and 24 h hours after L. infantum inoculation. In liver, the parasites were readily observed already at 1 h and 2 h after the infection. All parasites were localised close to or inside macrophages and no Leishmania were detected inside neutrophil cells, at any time of observation. In contrast, in spleen tissue, parasites were much less abundant and several fields had to be screened in order to find Leishmania. A part of spleen neutrophils was found to contain at least one parasite in a more or less degraded state. Figure 2 shows that within one hour post infection, the intraneutrophil protozoan, although recognised by parietal tubules, flagellar pocket and longitudinal-cut flagella, generally lost its ultrastructural integrity. The electron microscopy images do not at all instances allow determining the precise intracellular parasite localisation, so a quantitative evaluation in spleen of the percentage of parasitised macrophages versus parasitised neutrophils would be non-reliable. Twenty-four hours after the infection, neutrophil influx was still observed in the spleen (Figure 3) but no intraneutrophil parasites were detected. In the parasitised monocytes (Figure 4) Leishmania appeared relatively intact as compared to that phagocytised by PMN.

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Groupe de Recherche en Immunopathologie de la Leishmaniose (EA 2675),INSERM U364, IFR 50, Faculté de Médecine, 06107 Nice Cedex 2, France. droussea@unice.fr

ABSTRACT

Background: 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.

Results: 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.

Conclusions: 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.

Show MeSH
Related in: MedlinePlus