dc.creatorDuque, Thabata L. A.
dc.creatorSiqueira, Mariana S.
dc.creatorTravassos, Leonardo H.
dc.creatorMoreira, Otacilio C.
dc.creatorBozza, Patrícia T.
dc.creatorMelo, Rossana C. N.
dc.creatorHenriques-Pons, Andrea
dc.creatorMenna-Barreto, Rubem F. S.
dc.date2020-04-20T14:36:14Z
dc.date2020-04-20T14:36:14Z
dc.date2020
dc.date.accessioned2023-09-26T20:39:55Z
dc.date.available2023-09-26T20:39:55Z
dc.identifierDUQUE, Thabata L. A. et al. The induction of host cell autophagy triggers defense mechanisms against Trypanosoma cruzi infection in vitro. European Journal of Cell Biology, v. 99, p. 1-10, 2020.
dc.identifier0171-9335
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/40885
dc.identifier10.1016/j.ejcb.2019.151060
dc.identifier1618-1298
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8861594
dc.descriptionAcesso aberto em 20/04/2020 - hhtp;?https://reader.elsevier.com/reader/sd/pii/S017193351930144X?token=213749C9F9F6F455F65F32295E5545DA7946D0D5020A7B705D38BCBC1BBA38A627A33F1420BBF85ABEA98C394F096A45
dc.descriptionTrypanosoma cruzi causes Chagas disease, a neglected illness that affects millions of people worldwide, especially in Latin America. The balance between biochemical pathways triggered by the parasite and host cells response will ultimately define the progression of a life-threatening disease, justifying the efforts to understand cellular mechanisms for infection restrain. In this interaction, parasite and host cells are affected by different physiological responses as autophagy modulation, which could be under intense cellular stress, such as nutrient deprivation, hormone depletion, or infection. Autophagy is a constitutive pathway that leads to degradation of macromolecules and cellular structures and may induce cell death. In Trypanosoma cruzi infection, the relevance of host autophagy is controversial regarding in vitro parasite intracellular life cycle. In the present study, we evaluated host cell autophagy during T. cruzi infection in phagocytic and non-professional phagocytic cells. We described that the presence of the parasite increased the number of LC3 puncta, a marker for autophagy, in cardiac cells and peritoneal macrophages in vitro. The induction of host autophagy decreased infection in macrophages in early and late time-periods. We suggest that starved phagocytic cells reduced internalization, also confirmed by inert particles and dead trypomastigotes. Whereas, in cardiac cells, starvation-induced autophagy decreased lipid droplets and infection in later time-point, by reducing parasite differentiation/proliferation. In ATG5 knockout MEF cells, we confirmed our hypothesis of autophagy machinery activation during parasite internalization, increasing infection. Our data suggest that host autophagy downregulates T. cruzi infection through impairing parasite intracellular life cycle, reducing the infection in primary culture cells.
dc.description2025-01-01
dc.formatapplication/pdf
dc.languageeng
dc.publisherElsevier
dc.rightsrestricted access
dc.subjectTrypanosoma cruzi
dc.subjectAutofagia
dc.subjectInanição
dc.subjectCélula cardíaca
dc.subjectInteração da célula hospedeira
dc.subjectMacrófagos
dc.subjectTrypanosoma cruzi
dc.subjectAutophagy
dc.subjectStarvation
dc.subjectCardiac cell
dc.subjectMacrophage
dc.subjectHost cell interaction
dc.titleThe induction of host cell autophagy triggers defense mechanisms against Trypanosoma cruzi infection in vitro
dc.typeArticle


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