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Interactions with apoptotic but not with necrotic neutrophils increase parasite burden in human macrophages infected with Leishmania amazonensis
Author(s) -
Afonso Lilian,
Borges Valéria M.,
Cruz Heloísa,
RibeiroGomes Flávia L.,
DosReis George A.,
Dutra Alberto Noronha,
Clarêncio Jorge,
Oliveira Camila I.,
Barral Aldina,
BarralNetto Manoel,
Brodskyn Cláudia I.
Publication year - 2008
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0108018
Subject(s) - biology , parasite hosting , leishmania , apoptosis , microbiology and biotechnology , phagocytosis , macrophage , protozoa , immunology , in vitro , genetics , world wide web , computer science
Neutrophils are involved in the initial steps of most responses to pathogens. In the present study, we evaluated the effects of the interaction of apoptotic vs. necrotic human neutrophils on macrophage infection by Leishmania amazonensis . Phagocytosis of apoptotic, but not viable, neutrophils by Leishmania‐ infected macrophages led to an increase in parasite burden via a mechanism dependent on TGF‐β1 and PGE 2 . Conversely, infected macrophages’ uptake of necrotic neutrophils induced killing of L. amazonensis . Leishmanicidal activity was dependent on TNF‐α and neutrophilic elastase. Nitric oxide was not involved in the killing of parasites, but the interaction of necrotic neutrophils with infected macrophages resulted in high superoxide production, a process reversed by catalase, an inhibitor of reactive oxygen intermediate production. Initial events after Leishmania infection involve interactions with neutrophils; we demonstrate that phagocytosis of these cells in an apoptotic or necrotic stage can influence the outcome of infection, driving either parasite survival or destruction.