| Author | Gomes, Flávia Lima Ribeiro | |
| Author | Souza, Maria Carolina Abieri Moniz de | |
| Author | Borges, Valeria de Matos | |
| Author | Nunes, Marise Pinheiro | |
| Author | Barradas, Marcio Mantuano | |
| Author | Bizarro, Heloisa D’Ávila da Silva | |
| Author | Bozza, Patrícia T. | |
| Author | Calich, Vera Lucia Garcia | |
| Author | DosReis, George Alexandre | |
| Access date | 2015-02-10T13:55:47Z | |
| Available date | 2015-02-10T13:55:47Z | |
| Document date | 2005 | |
| 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. | pt_BR |
| ISSN | 0022-1899 | |
| URI | https://www.arca.fiocruz.br/handle/icict/9471 | |
| Language | eng | pt_BR |
| Publisher | Oxford University Press | pt_BR |
| Rights | open access | pt_BR |
| Title | Turnover of neutrophils mediated by Fas ligand drives Leishmania major infection. | pt_BR |
| Type | Article | pt_BR |
| 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. | pt_BR |
| Affilliation | Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil | pt_BR |
| Affilliation | Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil | pt_BR |
| Affilliation | Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil | pt_BR |
| Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil | pt_BR |
| Affilliation | Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil | pt_BR |
| Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil | pt_BR |
| Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil | pt_BR |
| Affilliation | University of São Paulo. Instituto de Ciências Biomédicas. São Paulo, SP, Brasil | pt_BR |
| Affilliation | Federal University of Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil | pt_BR |
| DeCS | Leishmania major/crescimento & desenvolvimento | pt_BR |
| DeCS | Leishmania major/imunologia | pt_BR |
| DeCS | Leishmaniose Cutânea/imunologia | pt_BR |
| DeCS | Glicoproteínas de Membrana/imunologia | pt_BR |
| DeCS | Neutrófilos/imunologia | pt_BR |
| DeCS | Neutrófilos/patologia | pt_BR |
| DeCS | Animais | pt_BR |
| DeCS | Apoptose | pt_BR |
| DeCS | Morte Celular/imunologia | pt_BR |
| DeCS | Modelos Animais de Doenças | pt_BR |
| DeCS | Suscetibilidade a Doenças | pt_BR |
| DeCS | Proteína Ligante Fas | pt_BR |
| DeCS | Leishmaniose Cutânea/genética | pt_BR |
| DeCS | Camundongos | pt_BR |
| DeCS | Camundongos Endogâmicos BALB C | pt_BR |
| DeCS | Camundongos Knockout | pt_BR |
