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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.

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Related in: MedlinePlus

Trypanosoma cruzi infection induces concomitant lipid body formation and prostaglandin E2 (PGE2) synthesis. Associations between number of lipid bodies (bars) and prostaglandin E2 (PGE2) peritoneal levels (line) in rats at day 6 or 12 of infection with T. cruzi and in uninfected controls. At both days, the lipid body numbers were significantly increased (P < 0.05) in parallel to an accentuated increase of PGE2 synthesis. Data are expressed as means ± SEM. Reprinted from [11] with permission.
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fig5: Trypanosoma cruzi infection induces concomitant lipid body formation and prostaglandin E2 (PGE2) synthesis. Associations between number of lipid bodies (bars) and prostaglandin E2 (PGE2) peritoneal levels (line) in rats at day 6 or 12 of infection with T. cruzi and in uninfected controls. At both days, the lipid body numbers were significantly increased (P < 0.05) in parallel to an accentuated increase of PGE2 synthesis. Data are expressed as means ± SEM. Reprinted from [11] with permission.

Mentions: The increased formation of lipid bodies within inflammatory macrophages is accompanied by significant production of the PGE2. The highest numbers of lipid bodies induced by the T. cruzi infection in inflammatory macrophages occurred in parallel to the highest production of PGE2 [11] (Figure 5). This increase was documented at days 6 (fourfold) and 12 (sixfold) after infection in rats [11] (Figure 5). In murine model, the increased PGE2 production derived from lipid bodies was rapidly observed at 24 h of infection (fourfold), through a TLR2-dependent manner [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 concomitant lipid body formation and prostaglandin E2 (PGE2) synthesis. Associations between number of lipid bodies (bars) and prostaglandin E2 (PGE2) peritoneal levels (line) in rats at day 6 or 12 of infection with T. cruzi and in uninfected controls. At both days, the lipid body numbers were significantly increased (P < 0.05) in parallel to an accentuated increase of PGE2 synthesis. Data are expressed as means ± SEM. Reprinted from [11] with permission.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig5: Trypanosoma cruzi infection induces concomitant lipid body formation and prostaglandin E2 (PGE2) synthesis. Associations between number of lipid bodies (bars) and prostaglandin E2 (PGE2) peritoneal levels (line) in rats at day 6 or 12 of infection with T. cruzi and in uninfected controls. At both days, the lipid body numbers were significantly increased (P < 0.05) in parallel to an accentuated increase of PGE2 synthesis. Data are expressed as means ± SEM. Reprinted from [11] with permission.
Mentions: The increased formation of lipid bodies within inflammatory macrophages is accompanied by significant production of the PGE2. The highest numbers of lipid bodies induced by the T. cruzi infection in inflammatory macrophages occurred in parallel to the highest production of PGE2 [11] (Figure 5). This increase was documented at days 6 (fourfold) and 12 (sixfold) after infection in rats [11] (Figure 5). In murine model, the increased PGE2 production derived from lipid bodies was rapidly observed at 24 h of infection (fourfold), through a TLR2-dependent manner [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