Limits...
Lipid bodies: inflammatory organelles implicated in host-Trypanosoma cruzi interplay during innate immune responses.

D'Avila H, Toledo DA, Melo RC - Mediators Inflamm. (2012)

Bottom Line: A distinguishing feature of Chagas' disease-triggered macrophages is the presence of increased numbers of distinct cytoplasmic organelles termed lipid bodies or lipid droplets.These organelles are actively formed in response to the parasite and are sites for synthesis and storage of inflammatory mediators.The increased knowledge of lipid bodies in pathogenic mechanisms of infections may not only contribute to the understanding of pathogen-host interactions but may also identify new targets for intervention.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Cellular Biology, Department of Biology, Federal University of Juiz de Fora (UF JF), 36036-900 Juiz de Fora, MG, Brazil.

ABSTRACT
The flagellated protozoa Trypanosoma cruzi is the causal agent of Chagas' disease, a significant public health issue and still a major cause of morbidity and mortality in Latin America. Acute Chagas' disease elicits a strong inflammatory response. In order to control the parasite multiplication, cells of the monocytic lineage are highly mobilized. Monocyte differentiation leads to the formation of phagocytosing macrophages, which are strongly activated and direct host defense. A distinguishing feature of Chagas' disease-triggered macrophages is the presence of increased numbers of distinct cytoplasmic organelles termed lipid bodies or lipid droplets. These organelles are actively formed in response to the parasite and are sites for synthesis and storage of inflammatory mediators. This review covers current knowledge on lipid bodies elicited by the acute Chagas' disease within inflammatory macrophages and discusses the role of these organelles in inflammation. The increased knowledge of lipid bodies in pathogenic mechanisms of infections may not only contribute to the understanding of pathogen-host interactions but may also identify new targets for intervention.

Show MeSH

Related in: MedlinePlus

Trypanosoma cruzi infection induces macrophage lipid body formation. Peritoneal macrophages isolated from mice were cultured or not with T. cruzi and the formation of lipid bodies analyzed after 24 h by staining with BODIPY 493/503 (a and b), a fluorescent lipid probe for highly hydrophobic environments [35] or osmium tetroxide (c and d). While uninfected cells (a, c) have small number of lipid bodies, infected cells (b and d) show increased number of these organelles. Lipid bodies are seen as green (a and b) or brownish (c and d), round organelles. Nuclei of macrophages and internalized parasites (arrows) were stained with DAPI (4′,6-diamidino-2-phenylindole; blue). Scale bar, 10 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3350868&req=5

fig3: Trypanosoma cruzi infection induces macrophage lipid body formation. Peritoneal macrophages isolated from mice were cultured or not with T. cruzi and the formation of lipid bodies analyzed after 24 h by staining with BODIPY 493/503 (a and b), a fluorescent lipid probe for highly hydrophobic environments [35] or osmium tetroxide (c and d). While uninfected cells (a, c) have small number of lipid bodies, infected cells (b and d) show increased number of these organelles. Lipid bodies are seen as green (a and b) or brownish (c and d), round organelles. Nuclei of macrophages and internalized parasites (arrows) were stained with DAPI (4′,6-diamidino-2-phenylindole; blue). Scale bar, 10 μm.

Mentions: In vitro, lipid body accumulation has been observed within peritoneal macrophages isolated from mice and cultured with T. cruzi for 24 h [35] (Figures 3(a)–3(d)). At this time of infection, both the cells containing internalized parasites as well nonparasitized cells show increased number of lipid bodies compared to control, noninfected cells, suggesting a bystander amplification of the response (Figure 3(b)). Interestingly, parasitized cells show significant higher number of lipid bodies (threefold) compared to nonparasitized cells, indicating that the uptake of the parasite directly induces formation of lipid bodies [35] (Figure 3(b)). D'Avila and colleagues have also demonstrated that lipid body formation in macrophages in response to the T. cruzi infection occurs through a Toll-like receptor-2- (TLR2-) dependent mechanism, demonstrating a mechanism involving surface receptors in this event [35].


Lipid bodies: inflammatory organelles implicated in host-Trypanosoma cruzi interplay during innate immune responses.

D'Avila H, Toledo DA, Melo RC - Mediators Inflamm. (2012)

Trypanosoma cruzi infection induces macrophage lipid body formation. Peritoneal macrophages isolated from mice were cultured or not with T. cruzi and the formation of lipid bodies analyzed after 24 h by staining with BODIPY 493/503 (a and b), a fluorescent lipid probe for highly hydrophobic environments [35] or osmium tetroxide (c and d). While uninfected cells (a, c) have small number of lipid bodies, infected cells (b and d) show increased number of these organelles. Lipid bodies are seen as green (a and b) or brownish (c and d), round organelles. Nuclei of macrophages and internalized parasites (arrows) were stained with DAPI (4′,6-diamidino-2-phenylindole; blue). Scale bar, 10 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3350868&req=5

fig3: Trypanosoma cruzi infection induces macrophage lipid body formation. Peritoneal macrophages isolated from mice were cultured or not with T. cruzi and the formation of lipid bodies analyzed after 24 h by staining with BODIPY 493/503 (a and b), a fluorescent lipid probe for highly hydrophobic environments [35] or osmium tetroxide (c and d). While uninfected cells (a, c) have small number of lipid bodies, infected cells (b and d) show increased number of these organelles. Lipid bodies are seen as green (a and b) or brownish (c and d), round organelles. Nuclei of macrophages and internalized parasites (arrows) were stained with DAPI (4′,6-diamidino-2-phenylindole; blue). Scale bar, 10 μm.
Mentions: In vitro, lipid body accumulation has been observed within peritoneal macrophages isolated from mice and cultured with T. cruzi for 24 h [35] (Figures 3(a)–3(d)). At this time of infection, both the cells containing internalized parasites as well nonparasitized cells show increased number of lipid bodies compared to control, noninfected cells, suggesting a bystander amplification of the response (Figure 3(b)). Interestingly, parasitized cells show significant higher number of lipid bodies (threefold) compared to nonparasitized cells, indicating that the uptake of the parasite directly induces formation of lipid bodies [35] (Figure 3(b)). D'Avila and colleagues have also demonstrated that lipid body formation in macrophages in response to the T. cruzi infection occurs through a Toll-like receptor-2- (TLR2-) dependent mechanism, demonstrating a mechanism involving surface receptors in this event [35].

Bottom Line: A distinguishing feature of Chagas' disease-triggered macrophages is the presence of increased numbers of distinct cytoplasmic organelles termed lipid bodies or lipid droplets.These organelles are actively formed in response to the parasite and are sites for synthesis and storage of inflammatory mediators.The increased knowledge of lipid bodies in pathogenic mechanisms of infections may not only contribute to the understanding of pathogen-host interactions but may also identify new targets for intervention.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Cellular Biology, Department of Biology, Federal University of Juiz de Fora (UF JF), 36036-900 Juiz de Fora, MG, Brazil.

ABSTRACT
The flagellated protozoa Trypanosoma cruzi is the causal agent of Chagas' disease, a significant public health issue and still a major cause of morbidity and mortality in Latin America. Acute Chagas' disease elicits a strong inflammatory response. In order to control the parasite multiplication, cells of the monocytic lineage are highly mobilized. Monocyte differentiation leads to the formation of phagocytosing macrophages, which are strongly activated and direct host defense. A distinguishing feature of Chagas' disease-triggered macrophages is the presence of increased numbers of distinct cytoplasmic organelles termed lipid bodies or lipid droplets. These organelles are actively formed in response to the parasite and are sites for synthesis and storage of inflammatory mediators. This review covers current knowledge on lipid bodies elicited by the acute Chagas' disease within inflammatory macrophages and discusses the role of these organelles in inflammation. The increased knowledge of lipid bodies in pathogenic mechanisms of infections may not only contribute to the understanding of pathogen-host interactions but may also identify new targets for intervention.

Show MeSH
Related in: MedlinePlus