Macrophages induce neutrophil apoptosis through membrane TNF, a process amplified by Leishmania major.

Détails

ID Serval
serval:BIB_10B818058C4D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Macrophages induce neutrophil apoptosis through membrane TNF, a process amplified by Leishmania major.
Périodique
Journal of Immunology
Auteur(s)
Allenbach C., Zufferey C., Perez C., Launois P., Mueller C., Tacchini-Cottier F.
ISSN
0022-1767 (Print)
ISSN-L
0022-1767
Statut éditorial
Publié
Date de publication
2006
Volume
176
Numéro
11
Pages
6656-6664
Langue
anglais
Résumé
Neutrophils are recruited to the site of parasite inoculation within a few hours of infection with the protozoan parasite Leishmania major. In C57BL/6 mice, which are resistant to infection, neutrophils are cleared from the site of s.c. infection within 3 days, whereas they persist for at least 10 days in susceptible BALB/c mice. In the present study, we investigated the role of macrophages (MPhi) in regulating neutrophil number. Inflammatory cells were recruited by i.p. injection of either 2% starch or L. major promastigotes. Neutrophils were isolated and cultured in the presence of increasing numbers of MPhi. Extent of neutrophil apoptosis positively correlated with the number of MPhi added. This process was strictly dependent on TNF because MPhi from TNF-deficient mice failed to induce neutrophil apoptosis. Assays using MPhi derived from membrane TNF knock-in mice or cultures in Transwell chambers revealed that contact with MPhi was necessary to induce neutrophil apoptosis, a process requiring expression of membrane TNF. L. major was shown to exacerbate MPhi-induced apoptosis of neutrophils, but BALB/c MPhi were not as potent as C57BL/6 MPhi in this induction. Our results emphasize the importance of MPhi-induced neutrophil apoptosis, and membrane TNF in the early control of inflammation.
Mots-clé
Animals, Apoptosis/immunology, Cell Communication/genetics, Cell Communication/immunology, Cells, Cultured, Coculture Techniques, Female, Inflammation Mediators/metabolism, Inflammation Mediators/physiology, Leishmania major/immunology, Leukocyte Count, Macrophages, Peritoneal/immunology, Macrophages, Peritoneal/metabolism, Membrane Proteins/physiology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Neutrophils/cytology, Neutrophils/immunology, Species Specificity, Time Factors, Tumor Necrosis Factor-alpha/deficiency, Tumor Necrosis Factor-alpha/genetics
Pubmed
Web of science
Création de la notice
24/01/2008 16:09
Dernière modification de la notice
20/08/2019 13:37
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