Histological Approaches to Study Tissue Parasitism During the Experimental Trypanosoma cruzi Infection

Fabrino, Daniela Leite; Ribeiro, Grazielle Alves; Teixeira, Lívia; Melo, Rossana C. N.

doi:10.1007/978-1-60761-950-5_5

Cited by 2 publications

(2 citation statements)

References 15 publications

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“…For the quantification of cardiac amastigotes nests, six semi-serial sections with 70-μm intervals, were obtained for each heart and stained with hematoxylin-eosin [61]. Twenty five (25) slices per field were analyzed by conventional microscopy using an Olympus CX31 microscope.…”

Section: Histopathologymentioning

confidence: 99%

Autophagy plays a protective role against Trypanosoma cruzi infection in mice

et al. 2019

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Autophagy is a catabolic pathway required for cellular and organism homeostasis. Autophagy participates in the innate and adaptive immune responses at different levels. Xenophagy is a class of selective autophagy that involves the elimination of intracellular pathogens. Trypanosoma cruzi is the causative agent of Chagas, a disease that affects 8 million individuals worldwide. Previously, our group has demonstrated that autophagy participates in the invasion of T. cruzi in non-phagocytic cells. In this work we have studied the involvement of autophagy in the development of T. cruzi infection in mice. Beclin-1 is a protein essential for autophagy, required for autophagosome biogenesis and maturation. We have performed an acute model of infection on the autophagic deficient Beclin-1 heterozygous knock-out mice (Bcln ± ) and compared to control Bcln +/+ animals. In addition, we have analyzed the infection process in both peritoneal cells and RAW macrophages. Our results have shown that the infection was more aggressive in the autophagy-deficient mice, which displayed higher numbers of parasitemia, heart´s parasitic nests and mortality rates. We have also found that peritoneal cells derived from Bcln ± animals and RAW macrophages treated with autophagy inhibitors displayed higher levels of infection compared to controls. Interestingly, free cytosolic parasites recruited LC3 protein and other markers of xenophagy in control compared to autophagy-deficient cells. Taken together, these data suggest that autophagy plays a protective role against T. cruzi infection in mice, xenophagy being one of the processes activated as part of the repertoire of immune responses generated by the host.

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Section: Histopathologymentioning

confidence: 99%

Autophagy plays a protective role against Trypanosoma cruzi infection in mice

et al. 2019

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“…In (b), nests of amastigotes (arrows), the intracellular form of the parasite, and inflammatory processes (circles) characterized by predominance of mononuclear cells are observed in the myocardium (My). Semi-serial 5 μ m-thick sections of the heart were cut, stained by haematoxylin and eosin and examined for qualitative evaluation of the inflammatory and degenerative processes and quantification of parasitism [8, 34]. In (c), an electron micrograph of a parasitized cardiomyocyte (c) showing vacuoles (V) and many amastigotes (A).…”

Section: Figurementioning

confidence: 99%

Lipid Bodies: Inflammatory Organelles Implicated in Host-Trypanosoma cruziInterplay during Innate Immune Responses

D’Avila

Toledo

Melo

2012

Mediators of Inflammation

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The flagellated protozoaTrypanosoma cruziis 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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Histological Approaches to Study Tissue Parasitism During the Experimental Trypanosoma cruzi Infection

Cited by 2 publications

References 15 publications

Autophagy plays a protective role against Trypanosoma cruzi infection in mice

Autophagy plays a protective role against Trypanosoma cruzi infection in mice

Lipid Bodies: Inflammatory Organelles Implicated in Host-Trypanosoma cruziInterplay during Innate Immune Responses

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