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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

Lipid bodies (LB) within heart inflammatory macrophages increase in size in response to acute Trypanosoma cruzi infection and parasite load. (a) Strongly electron dense LBs from an infected animal are observed in the cytoplasm n conjunction with free amastigote forms of the parasite (asterisks). In (b), a giant LB is seen close to the nucleus in an irradiated-infected rat. (c) LB diameter variation in different groups. A significant increase of LB occurred in infected alone compared to uninfected and in irradiated-infected compared to infected alone groups (P < 0.05). Before infection, rats were irradiated or not and heart samples processed for transmission electron microscopy at day 12 of infection. Scale bar, 1.0 μm (a); 600 nm (b). Reprinted from [29] with permission.
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fig4: Lipid bodies (LB) within heart inflammatory macrophages increase in size in response to acute Trypanosoma cruzi infection and parasite load. (a) Strongly electron dense LBs from an infected animal are observed in the cytoplasm n conjunction with free amastigote forms of the parasite (asterisks). In (b), a giant LB is seen close to the nucleus in an irradiated-infected rat. (c) LB diameter variation in different groups. A significant increase of LB occurred in infected alone compared to uninfected and in irradiated-infected compared to infected alone groups (P < 0.05). Before infection, rats were irradiated or not and heart samples processed for transmission electron microscopy at day 12 of infection. Scale bar, 1.0 μm (a); 600 nm (b). Reprinted from [29] with permission.

Mentions: As noted, the accumulation of newly recruited macrophages in the heart is one of the main findings of the acute T. cruzi infection and it is correlated with the intense myocardium parasitism which occurs during the early infection in both experimental models and humans (reviewed in [6]) (Figure 2). At day 12 of T. cruzi infection in rats, is observed the most intense inflammatory process and parasitism in the heart compared to other points during the acute phase [7]. Ultrastructural analysis of this organ showed numerous infiltrating macrophages with lipid bodies prominently increased in number and size [11] (Figure 4(a)). Inflammatory heart macrophages, evaluated by quantitative electron microscopy, exhibited a mean of 8.3 lipid bodies/cell section (range of 1–25) at the same time of infection whereas control noninflammatory macrophages showed a mean of 2.6 lipid bodies/cell section (range of 0–3) [11].


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

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

Lipid bodies (LB) within heart inflammatory macrophages increase in size in response to acute Trypanosoma cruzi infection and parasite load. (a) Strongly electron dense LBs from an infected animal are observed in the cytoplasm n conjunction with free amastigote forms of the parasite (asterisks). In (b), a giant LB is seen close to the nucleus in an irradiated-infected rat. (c) LB diameter variation in different groups. A significant increase of LB occurred in infected alone compared to uninfected and in irradiated-infected compared to infected alone groups (P < 0.05). Before infection, rats were irradiated or not and heart samples processed for transmission electron microscopy at day 12 of infection. Scale bar, 1.0 μm (a); 600 nm (b). Reprinted from [29] with permission.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Lipid bodies (LB) within heart inflammatory macrophages increase in size in response to acute Trypanosoma cruzi infection and parasite load. (a) Strongly electron dense LBs from an infected animal are observed in the cytoplasm n conjunction with free amastigote forms of the parasite (asterisks). In (b), a giant LB is seen close to the nucleus in an irradiated-infected rat. (c) LB diameter variation in different groups. A significant increase of LB occurred in infected alone compared to uninfected and in irradiated-infected compared to infected alone groups (P < 0.05). Before infection, rats were irradiated or not and heart samples processed for transmission electron microscopy at day 12 of infection. Scale bar, 1.0 μm (a); 600 nm (b). Reprinted from [29] with permission.
Mentions: As noted, the accumulation of newly recruited macrophages in the heart is one of the main findings of the acute T. cruzi infection and it is correlated with the intense myocardium parasitism which occurs during the early infection in both experimental models and humans (reviewed in [6]) (Figure 2). At day 12 of T. cruzi infection in rats, is observed the most intense inflammatory process and parasitism in the heart compared to other points during the acute phase [7]. Ultrastructural analysis of this organ showed numerous infiltrating macrophages with lipid bodies prominently increased in number and size [11] (Figure 4(a)). Inflammatory heart macrophages, evaluated by quantitative electron microscopy, exhibited a mean of 8.3 lipid bodies/cell section (range of 1–25) at the same time of infection whereas control noninflammatory macrophages showed a mean of 2.6 lipid bodies/cell section (range of 0–3) [11].

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