Uptake of apoptotic cells drives the growth of a pathogenic trypanosome in macrophages

Célio G. Freire- de-Lima, Danielle O. Nascimento, Milena B. P. Soares, Patricia T. Bozza, Hugo C. Castro-Faria-Neto, Fernando G. de Mello, George A. DosReis () and Marcela F. Lopes ()
Additional contact information
Célio G. Freire- de-Lima: Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro
Danielle O. Nascimento: Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro
Milena B. P. Soares: Centro de Pesquisas Gonçalo Moniz, FIOCRUZ
Patricia T. Bozza: Instituto Oswaldo Cruz, FIOCRUZ
Hugo C. Castro-Faria-Neto: Instituto Oswaldo Cruz, FIOCRUZ
Fernando G. de Mello: Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro
George A. DosReis: Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro
Marcela F. Lopes: Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro

Nature, 2000, vol. 403, issue 6766, 199-203

Abstract: Abstract After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells1. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages2,3. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease4, 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-β (TGF-β) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E2/TGF-β 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.

Date: 2000
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/35003208 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:403:y:2000:i:6766:d:10.1038_35003208

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/35003208

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().