Author | Lima, Celio Geraldo Freire de | |
Author | Nascimento, Danielle de Oliveira | |
Author | Soares, Milena Botelho Pereira | |
Author | Bozza, Patrícia Torres | |
Author | Faria Neto, Hugo Caire de Castro | |
Author | Mello, Fernando G. de | |
Author | DosReis, George Alexandre | |
Author | Lopes, Marcela de Freitas | |
Access date | 2015-04-07T16:30:54Z | |
Available date | 2015-04-07T16:30:54Z | |
Document date | 2000 | |
Citation | Freirde-Lima, C. G. et al. Uptake of apoptotic cells drives the growth of a pathogenic trypanosome in macrophages. Nature, v. 403, n. 6766, p. 199-203, 2000. | pt_BR |
ISSN | 0028-0836 | |
URI | https://www.arca.fiocruz.br/handle/icict/9910 | |
Language | eng | pt_BR |
Publisher | Macmillan Magazines Ltd | pt_BR |
Rights | open access | pt_BR |
Title | Uptake of apoptotic cells drives the growth of a pathogenic trypanosome in macrophages. | pt_BR |
Type | Article | pt_BR |
Abstract | After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease, a debilitating cardiac illness caused by the protozoan Trypanosoma cruzi. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with T. cruzi fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-beta (TGF-beta) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E2/TGF-beta release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it in vivo. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease. | pt_BR |
Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil | pt_BR |
Affilliation | Universidade Federal do 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 | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil | pt_BR |
Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil | pt_BR |
Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil | pt_BR |
Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil | pt_BR |
DeCS | Apoptose | pt_BR |
DeCS | Macrófagos/parasitologia | pt_BR |
DeCS | Linfócitos T/fisiologia | pt_BR |
DeCS | Trypanosoma cruzi/crescimento & desenvolvimento | pt_BR |
DeCS | Clorometilcetonas de Aminoácidos/farmacologia | pt_BR |
DeCS | Animais | pt_BR |
DeCS | Células Cultivadas | pt_BR |
DeCS | Doença de Chagas/imunologia | pt_BR |
DeCS | Inibidores de Cisteína Proteinase/farmacologia | pt_BR |
DeCS | Dinoprostona/biossíntese | pt_BR |
DeCS | Masculino | pt_BR |
DeCS | Camundongos | pt_BR |
DeCS | Camundongos Endogâmicos BALB C | pt_BR |
DeCS | Necrose | pt_BR |
DeCS | Fagocitose/fisiologia | pt_BR |
DeCS | Putrescina/biossíntese | pt_BR |
DeCS | Receptores de Vitronectina/metabolismo | pt_BR |
DeCS | Linfócitos T/efeitos de drogas | pt_BR |
DeCS | Fator de Crescimento Transformador beta/fisiologia | pt_BR |