Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 204, Issue 6, Pages 951-961Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jir432
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- PAPES-FIOCRUZ
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq, Brazil)
- Fundacao de Amparo a Pesquisa do Rio de Janeiro (FAPERJ, Brazil)
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Lipid bodies (lipid droplets) are lipid-rich organelles with functions in cell metabolism and signaling. Here, we investigate the mechanisms of Trypanosoma cruzi-induced lipid body formation and their contributions to host-parasite interplay. We demonstrate that T. cruzi-induced lipid body formation in macrophages occurs in a Toll-like receptor 2-dependent mechanism and is potentiated by apoptotic cell uptake. Lipid body biogenesis and prostaglandin E-2 (PGE(2)) production triggered by apoptotic cell uptake was largely dependent of alpha(v)beta(3) and transforming growth factor-beta signaling. T. cruzi-induced lipid bodies act as sites of increased PGE(2) synthesis. Inhibition of lipid body biogenesis by the fatty acid synthase inhibitor C75 reversed the effects of apoptotic cells on lipid body formation, eicosanoid synthesis, and parasite replication. Our findings indicate that lipid bodies are highly regulated organelles during T. cruzi infection with roles in lipid mediator generation by macrophages and are potentially involved in T. cruzi-triggered escape mechanisms.
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