Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/9471
Title: Turnover of neutrophils mediated by Fas ligand drives Leishmania major infection.
Authors: Gomes, Flávia Lima Ribeiro
Souza, Maria Carolina Abieri Moniz de
Borges, Valeria de Matos
Nunes, Marise Pinheiro
Barradas, Marcio Mantuano
Bizarro, Heloisa D’Ávila da Silva
Bozza, Patrícia Torres
Calich, Vera Lucia Garcia
DosReis, George Alexandre
Affilliation: Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil
Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
University of São Paulo. Instituto de Ciências Biomédicas. São Paulo, SP, Brasil
Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil
Abstract: Apoptosis mediated by Fas ligand (FasL) initiates inflammation characterized by neutrophilic infiltration. Neutrophils undergo apoptosis and are ingested by macrophages. Clearance of dead neutrophils leads to prostaglandin- and transforming growth factor-beta-dependent replication of Leishmania major in macrophages from susceptible mice. How L. major induces neutrophil turnover in a physiological setting is unknown. We show that BALB/c FasL-sufficient mice are more susceptible to L. major infection than are FasL-deficient mice. FasL promotes the apoptosis of infected resident macrophages and attracts neutrophils. Furthermore, FasL-sufficient neutrophils exacerbate L. major replication in macrophages, whereas FasL-deficient neutrophils induce parasite killing. These contrasting effects are due to delaying apoptosis and the clearance of FasL-deficient neutrophils. The transfer of neutrophils exacerbates infection in FasL-sufficient mice but reduces infection in FasL-deficient mice. Depletion of neutrophils abolishes the susceptibility of FasL-sufficient mice. These data illustrate a deleterious role of the FasL-mediated turnover of neutrophils on L. major infection.
DeCS: Leishmania major/crescimento & desenvolvimento
Leishmania major/imunologia
Leishmaniose Cutânea/imunologia
Glicoproteínas de Membrana/imunologia
Neutrófilos/imunologia
Neutrófilos/patologia
Animais
Apoptose
Morte Celular/imunologia
Modelos Animais de Doenças
Suscetibilidade a Doenças
Proteína Ligante Fas
Leishmaniose Cutânea/genética
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Issue Date: 2005
Publisher: Oxford University Press
Citation: RIBEIRO-GOMES, F. L. et al. Turnover of neutrophils mediated by Fas ligand drives Leishmania major infection. Journal of Infectious Diseases, v. 192, n. 6, p. 1127-1134, 2005.
ISSN: 0022-1899
Copyright: open access
Appears in Collections:BA - IGM - Artigos de Periódicos

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