Macrophage lipid body induction by Chagas disease in vivo: putative intracellular domains for eicosanoid formation during infection

Melo, Rossana C. N.; D’Avila, Heloísa; Fabrino, Daniela Leite; Almeida, Patrícia E. de; Bozza, Patrı́cia T.

doi:10.1016/s0040-8166(02)00105-2

Cited by 102 publications

(152 citation statements)

References 37 publications

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“…The leukocytic infiltrate consists mainly of lymphocytes, and to a lesser extent macrophages, eosinophils, plasma cells, neutrophils and mast cells [4,[9][10][11]. Although the precise contribution of each of these cell types remains speculative, several lines of evidence suggest an important role for eosinophils and neutrophils in CHD pathogenesis.…”

Section: Antibody-mediated Cytotoxicity and Non-specific Damage Causementioning

confidence: 99%

“…The inflammatory infiltrate characteristic of CHD consists mainly of lymphocytes, with T cells predominating in a 3:1 ratio of CD8 + to CD4 + cells [8]. Macrophages, eosinophils, plasma cells, neutrophils and mast cells are also present to a lesser extent [4,[9][10][11]. T. cruzi infection influences the cytokine milieu by eliciting prolific production of type I cytokines such as IFN-γ, IL-12, and TNF-α and by regulatory type II cytokines such as IL-4 and IL-10 [3].…”

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confidence: 99%

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Chagas Heart Disease Pathogenesis: One Mechanism or Many?

Bonney

Engman²

2008

CMM

151

144

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Chagas heart disease (CHD), caused by the protozoan parasite Trypanosoma cruzi, is the leading cause of infectious myocarditis in the world. The etiology of CHD is unclear and multiple mechanisms have been proposed to explain the pathogenesis of the disease. This review describes the proposed mechanisms of CHD pathogenesis and evaluates the historical significance and evidence supporting each. Although the majority of CHD-related pathologies are currently attributed to parasite persistence in the myocardium and autoimmunity, there is strong evidence that CHD develops as a result of additive and even synergistic effects of several distinct mechanisms rather than one factor.

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Section: Antibody-mediated Cytotoxicity and Non-specific Damage Causementioning

confidence: 99%

mentioning

confidence: 99%

Chagas Heart Disease Pathogenesis: One Mechanism or Many?

Bonney

Engman²

2008

CMM

151

144

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“…This cytoplasmic inclusion is constitutive in several myeloid cells, including eosinophils, neutrophils, and monocytes, and increased numbers of lipid bodies are found in cells associated with natural or experimentally induced inflammatory process (22,(37)(38)(39)(40)(41)(42). Lipid body formation can be induced by different stimuli, including CC chemokines through activation of CCR3 (43), arachidonic acid, oleic acid, and PAF (20,21,44).…”

Section: Discussionmentioning

confidence: 99%

Synergism Between Platelet-Activating Factor-Like Phospholipids and Peroxisome Proliferator-Activated Receptor γ Agonists Generated During Low Density Lipoprotein Oxidation That Induces Lipid Body Formation in Leukocytes

Assis

Silva

Caiado

et al. 2003

The Journal of Immunology

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Oxidized low density lipoprotein (LDL) has an important proinflammatory role in atherogenesis. In this study, we investigated the ability of oxidized LDL (oxLDL) and its phospholipid components to induce lipid body formation in leukocytes. Incubation of mouse peritoneal macrophages with oxidized, but not with native LDL led to lipid body formation within 1 h. This was blocked by platelet-activating factor (PAF) receptor antagonists or by preincubation of oxLDL with rPAF acetylhydrolase. HPLC fractions of phospholipids purified from oxLDL induced calcium flux in neutrophils as well as lipid body formation in macrophages. Injection of the bioactive phospholipid fractions or butanoyl and butenoyl PAF, a phospholipid previously shown to be present in oxLDL, into the pleural cavity of mice induced lipid body formation in leukocytes recovered after 3 h. The 5-lipoxygenase and cyclooxygenase-2 colocalized within lipid bodies formed after stimulation with oxLDL, bioactive phospholipid fractions, or butanoyl and butenoyl PAF. Lipid body formation was inhibited by 5-lipoxygenase antagonists, but not by cyclooxygenase-2 inhibitors. Azelaoyl-phosphatidylcholine, a peroxisome proliferator-activated receptor-γ agonist in oxLDL phospholipid fractions, induced formation of lipid bodies at late time points (6 h) and synergized with suboptimal concentrations of oxLDL. We conclude that lipid body formation is an important proinflammatory effect of oxLDL and that PAF-like phospholipids and peroxisome proliferator-activated receptor-γ agonists generated during LDL oxidation are important mediators in this phenomenon.

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“…In this regard, the number of LD has been shown to increase during the interaction of macrophages with pathogens, such as parasites (Melo et al, 2003), bacteria (Peyron et al, 2008;Daniel et al, 2011;Cardona et al, 2000;Tanigawa et al, 2008;Cao et al, 2007) and viruses (Barba et al, 1997;Samsa et al, 2009). Moreover, during infection, LD are mobilized into phagosomes, so the pathogen can use them as energy sources and for increased production of inflammatory mediators.…”

Section: Lipid Dropletsmentioning

confidence: 99%

Role of bioactive lipid mediators in obese adipose tissue inflammation and endocrine dysfunction

Lopategi

López‐Vicario

Alcaraz‐Quiles

et al. 2016

Molecular and Cellular Endocrinology

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a b s t r a c tWhite adipose tissue is recognized as an active endocrine organ implicated in the maintenance of metabolic homeostasis. However, adipose tissue function, which has a crucial role in the development of obesity-related comorbidities including insulin resistance and non-alcoholic fatty liver disease, is dysregulated in obese individuals. This review explores the physiological functions and molecular actions of bioactive lipids biosynthesized in adipose tissue including sphingolipids and phospholipids, and in particular fatty acids derived from phospholipids of the cell membrane. Special emphasis is given to polyunsaturated fatty acids of the omega-6 and omega-3 families and their conversion to bioactive lipid mediators through the cyclooxygenase and lipoxygenase pathways. The participation of omega-3-derived lipid autacoids in the resolution of adipose tissue inflammation and in the prevention of obesity-associated hepatic complications is also thoroughly discussed.

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Macrophage lipid body induction by Chagas disease in vivo: putative intracellular domains for eicosanoid formation during infection

Cited by 102 publications

References 37 publications

Chagas Heart Disease Pathogenesis: One Mechanism or Many?

Chagas Heart Disease Pathogenesis: One Mechanism or Many?

Synergism Between Platelet-Activating Factor-Like Phospholipids and Peroxisome Proliferator-Activated Receptor γ Agonists Generated During Low Density Lipoprotein Oxidation That Induces Lipid Body Formation in Leukocytes

Role of bioactive lipid mediators in obese adipose tissue inflammation and endocrine dysfunction

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