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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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Activation of heart inflammatory macrophages during the acute infection with Trypanosoma cruzi. In response to acute infections, a cascade of events recruits cells derived from monocytic lineage from the peripheral blood into heart. This cascade culminates in a strong activation of macrophages. Classical activation of macrophages involves the key cytokine interferon gamma (IFN-γ) and T. cruzi components (GPI anchors and CpG-rich DNA). These parasite products are recognized at the macrophage surface by Toll-like receptors (TLRs)-2 and 9, respectively. These receptors are a class of pattern recognition receptors (PRRs), which initiate an immune response and directly activates macrophages. Additionally, TLR-2 can heterodimerizate either TLR1 or TLR6 to recognize T. cruzi GPI anchors [33]. TNF-α is one of the most efficient activators of macrophages to a trypanocidal function. PAMPS, pathogen-associated molecular patterns; GPI, glycosyl phosphatidy linositol; TNF-α, tumor necrosis factor-alpha; MIP-1α, macrophage inflammatory protein α; MCP-1/CCL-2, monocyte chemoattractant protein-1; IP-10, inducible protein 10.
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fig1: Activation of heart inflammatory macrophages during the acute infection with Trypanosoma cruzi. In response to acute infections, a cascade of events recruits cells derived from monocytic lineage from the peripheral blood into heart. This cascade culminates in a strong activation of macrophages. Classical activation of macrophages involves the key cytokine interferon gamma (IFN-γ) and T. cruzi components (GPI anchors and CpG-rich DNA). These parasite products are recognized at the macrophage surface by Toll-like receptors (TLRs)-2 and 9, respectively. These receptors are a class of pattern recognition receptors (PRRs), which initiate an immune response and directly activates macrophages. Additionally, TLR-2 can heterodimerizate either TLR1 or TLR6 to recognize T. cruzi GPI anchors [33]. TNF-α is one of the most efficient activators of macrophages to a trypanocidal function. PAMPS, pathogen-associated molecular patterns; GPI, glycosyl phosphatidy linositol; TNF-α, tumor necrosis factor-alpha; MIP-1α, macrophage inflammatory protein α; MCP-1/CCL-2, monocyte chemoattractant protein-1; IP-10, inducible protein 10.

Mentions: Acute Chagas' disease elicits a strong inflammatory response. In order to control the parasite multiplication, cells of the monocytic lineage are highly mobilized (Figure 1). There is an intense migration and extravasation of monocytes from the bloodstream into target organs, mainly the heart (Figures 1 and 2). Monocyte differentiation leads to the formation of phagocytosing macrophages, strongly activated and involved in inhibiting parasite replication in the myocardium and other tissues [7, 8] (Figure 1). The ability of activated macrophages to process and present antigens, produce cytokines, and provide costimulatory signals demonstrates their pivotal role in initiating immune responses. The importance of these cells to the host defense has been pointed out by us and other groups during the in vivo acute T. cruzi infection in both humans and experimental models [7–10].


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

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

Activation of heart inflammatory macrophages during the acute infection with Trypanosoma cruzi. In response to acute infections, a cascade of events recruits cells derived from monocytic lineage from the peripheral blood into heart. This cascade culminates in a strong activation of macrophages. Classical activation of macrophages involves the key cytokine interferon gamma (IFN-γ) and T. cruzi components (GPI anchors and CpG-rich DNA). These parasite products are recognized at the macrophage surface by Toll-like receptors (TLRs)-2 and 9, respectively. These receptors are a class of pattern recognition receptors (PRRs), which initiate an immune response and directly activates macrophages. Additionally, TLR-2 can heterodimerizate either TLR1 or TLR6 to recognize T. cruzi GPI anchors [33]. TNF-α is one of the most efficient activators of macrophages to a trypanocidal function. PAMPS, pathogen-associated molecular patterns; GPI, glycosyl phosphatidy linositol; TNF-α, tumor necrosis factor-alpha; MIP-1α, macrophage inflammatory protein α; MCP-1/CCL-2, monocyte chemoattractant protein-1; IP-10, inducible protein 10.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Activation of heart inflammatory macrophages during the acute infection with Trypanosoma cruzi. In response to acute infections, a cascade of events recruits cells derived from monocytic lineage from the peripheral blood into heart. This cascade culminates in a strong activation of macrophages. Classical activation of macrophages involves the key cytokine interferon gamma (IFN-γ) and T. cruzi components (GPI anchors and CpG-rich DNA). These parasite products are recognized at the macrophage surface by Toll-like receptors (TLRs)-2 and 9, respectively. These receptors are a class of pattern recognition receptors (PRRs), which initiate an immune response and directly activates macrophages. Additionally, TLR-2 can heterodimerizate either TLR1 or TLR6 to recognize T. cruzi GPI anchors [33]. TNF-α is one of the most efficient activators of macrophages to a trypanocidal function. PAMPS, pathogen-associated molecular patterns; GPI, glycosyl phosphatidy linositol; TNF-α, tumor necrosis factor-alpha; MIP-1α, macrophage inflammatory protein α; MCP-1/CCL-2, monocyte chemoattractant protein-1; IP-10, inducible protein 10.
Mentions: Acute Chagas' disease elicits a strong inflammatory response. In order to control the parasite multiplication, cells of the monocytic lineage are highly mobilized (Figure 1). There is an intense migration and extravasation of monocytes from the bloodstream into target organs, mainly the heart (Figures 1 and 2). Monocyte differentiation leads to the formation of phagocytosing macrophages, strongly activated and involved in inhibiting parasite replication in the myocardium and other tissues [7, 8] (Figure 1). The ability of activated macrophages to process and present antigens, produce cytokines, and provide costimulatory signals demonstrates their pivotal role in initiating immune responses. The importance of these cells to the host defense has been pointed out by us and other groups during the in vivo acute T. cruzi infection in both humans and experimental models [7–10].

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