Interactions between Trypanosoma cruzi Secreted Proteins and Host Cell Signaling Pathways

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dc.citation.volume7
dc.contributor.authorCosta, Renata Watanabe [UNIEFSP]
dc.contributor.authorda Silveira, Jose F. [UNIFESP]
dc.contributor.authorBahia, Diana [UNIFESP]
dc.coverageLausanne
dc.date.accessioned2020-08-21T16:59:47Z
dc.date.available2020-08-21T16:59:47Z
dc.date.issued2016
dc.description.abstractChagas disease is one of the prevalent neglected tropical diseases, affecting at least 6-7 million individuals in Latin America. It is caused by the protozoan parasite Trypanosoma cruzi, which is transmitted to vertebrate hosts by blood-sucking insects. After infection, the parasite invades and multiplies in the myocardium, leading to acute myocarditis that kills around 5% of untreated individuals. T. cruzi secretes proteins that manipulate multiple host cell signaling pathways to promote host cell invasion. The primary secreted lysosomal peptidase in T. cruzi is cruzipain, which has been shown to modulate the host immune response. Cruzipain hinders macrophage activation during the early stages of infection by interrupting the NF-kB P65 mediated signaling pathway. This allows the parasite to survive and replicate, and may contribute to the spread of infection in acute Chagas disease. Another secreted protein P21, which is expressed in all of the developmental stages of T. cruzi, has been shown to modulate host phagocytosis signaling pathways. The parasite also secretes soluble factors that exert effects on host extracellular matrix, such as proteolytic degradation of collagens. Finally, secreted phospholipase A from T. cruzi contributes to lipid modifications on host cells and concomitantly activates the PKC signaling pathway. Here, we present a brief review of the interaction between secreted proteins from T cruzi and the host cells, emphasizing the manipulation of host signaling pathways during invasion.en
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Minas Gerais, Inst Ciencias Biol, Dept Biol Geral, Belo Horizonte, MG, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
dc.description.sponsorshipCoordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
dc.description.sponsorshipCNN
dc.description.sponsorshipIDFAPESP: 07/50551-2
dc.description.sponsorshipIDFAPESP: 11/51475-3
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.3389/fmicb.2016.00388
dc.identifier.citationFrontiers In Microbiology. Lausanne, v. 7, p. -, 2016.
dc.identifier.doi10.3389/fmicb.2016.00388
dc.identifier.fileWOS000373276000001.pdf
dc.identifier.issn1664-302X
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/57767
dc.identifier.wosWOS:000373276000001
dc.language.isoeng
dc.publisherFrontiers Media Sa
dc.relation.ispartofFrontiers In Microbiology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectT. cruzien
dc.subjectsecretomeen
dc.subjectsecreted proteinsen
dc.subjectvirulence factoren
dc.subjecthost parasite interactionen
dc.subjecthost cell signalingen
dc.subjecthost cell invasionen
dc.subjectChagas diseaseen
dc.titleInteractions between Trypanosoma cruzi Secreted Proteins and Host Cell Signaling Pathwaysen
dc.typeinfo:eu-repo/semantics/article
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