Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/32092
Title: Neutrophils recruited to the site of Mycobacterium bovis BCG infection undergo apoptosis and modulate lipid body biogenesis and prostaglandin E production by macrophages
Authors: D'Avila, Heloisa
Roque, Natalia R.
Cardoso, Rafael M.
Faria Neto, Hugo C. Castro
Melo, Rossana C. N.
Bozza, Patrícia T.
Affilliation: Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.
Universidade Federal de Juiz de Fora. Departamento de Biologia. Laboratório de Biologia Celular. Juiz de Fora, MG, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ. Brasil.
Abstract: Neutrophil influx to sites of mycobacterial infections is one of the first events of tuberculosis pathogenesis. However, the role of early neutrophil recruitment in mycobacterial infection is not completely understood. We investigated the rate of neutrophil apoptosis and the role of macrophage uptake of apoptotic neutrophils in a pleural tuberculosis model induced by BCG. Recruited neutrophils were shown to phagocyte BCG and a large number of neutrophils undergo apoptosis within 24 h. Notably, the great majority of apoptotic neutrophils were infected by BCG. Increased lipid body (lipid droplets) formation, accompanied by prostaglandin E(2) (PGE(2)) and TGF-beta1 synthesis, occurred in parallel to macrophage uptake of apoptotic cells. Lipid body and PGE(2) formation was observed after macrophage exposure to apoptotic, but not necrotic or live neutrophils. Blockage of BCG-induced lipid body formation significantly inhibited PGE(2) synthesis. Pre-treatment with the pan-caspase inhibitor zVAD inhibited BCG-induced neutrophil apoptosis and lipid body formation, indicating a role for apoptotic neutrophils in macrophage lipid body biogenesis in infected mice. In conclusion, BCG infection induced activation and apoptosis of infected neutrophils at the inflammatory site. The uptake of apoptotic neutrophils by macrophages leads to TGF-beta1 generation and PGE(2)-derived lipid body formation, and may have modulator roles in mycobacterial pathogenesis.
Keywords: Neutrophils
Mycobacterium bovis BCG
Infection
Tuberculosis
Lpid body
Macrophages
Apoptosis
prostaglandin E2 production
keywords: Neutrophils
Mycobacterium bovis BCG
Infecção
Tuberculose
Corpo liídico
Macrófagos
Apoptose
prostaglandina E2
Issue Date: 2008
Publisher: Wiley 12 Months
Citation: D`ÁVILA, Heloisa et al. Neutrophils recruited to the site of Mycobacterium bovis BCG infection undergo apoptosis and modulate lipid body biogenesis and prostaglandin E2 production by macrophages. Cellular Microbiology. v. 10, n. 12, p. 2589-2604, 2008.
DOI: 10.1111/j.1462-5822.2008.01233.x
ISSN: 1462-5814
Copyright: restricted access
Appears in Collections:IOC - Artigos de Periódicos

Files in This Item:
File Description SizeFormat 
D'Avila_RafaelCardoso_etal_IOC_2008.pdf963.94 kBAdobe PDF    Request a copy


FacebookTwitterDeliciousLinkedInGoogle BookmarksBibTex Format mendeley Endnote DiggMySpace

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.