Roles of Naturally Occurring Protease Inhibitors in the Modulation of Host Cell Signaling and Cellular Invasion by Trypanosoma cruzi

Scharfstein, Júlio; Lima, Ana Paula C. A.

doi:10.1007/978-0-387-78267-6_11

Cited by 25 publications

(25 citation statements)

References 81 publications

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“…Punctual damages to the basal lamina were also shown during the penetration of T. rangeli into R. prolixus and R. domesticus salivary glands [43], [44]. Given that proteases that are secreted or present on the surface of many protozoan parasites are involved in tissue invasion [45]–[50], we suggest that the altered morphology in the basal lamina of the O. fasciatus salivary glands was promoted by surface and/or secreted protease activities of P. serpens , which would aid in gland invasion by the parasites. In fact, our group has consistent evidence of the participation of P. serpens proteases in the interaction between this parasite and the salivary glands of O. fasciatus .…”

Section: Discussionmentioning

confidence: 99%

Evidence That a Laminin-Like Insect Protein Mediates Early Events in the Interaction of a Phytoparasite with Its Vector's Salivary Gland

et al. 2012

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Phytomonas species are plant parasites of the family Trypanosomatidae, which are transmitted by phytophagous insects. Some Phytomonas species cause major agricultural damages. The hemipteran Oncopeltus fasciatus is natural and experimental host for several species of trypanosomatids, including Phytomonas spp. The invasion of the insect vectors' salivary glands is one of the most important events for the life cycle of Phytomonas species. In the present study, we show the binding of Phytomonas serpens at the external face of O. fasciatus salivary glands by means of scanning electron microscopy and the in vitro interaction of living parasites with total proteins from the salivary glands in ligand blotting assays. This binding occurs primarily through an interaction with a 130 kDa salivary gland protein. The mass spectrometry of the trypsin-digest of this protein matched 23% of human laminin-5 β3 chain precursor sequence by 16 digested peptides. A protein sequence search through the transcriptome of O. fasciatus embryo showed a partial sequence with 51% similarity to human laminin β3 subunit. Anti-human laminin-5 β3 chain polyclonal antibodies recognized the 130 kDa protein by immunoblotting. The association of parasites with the salivary glands was strongly inhibited by human laminin-5, by the purified 130 kDa insect protein, and by polyclonal antibodies raised against the human laminin-5 β3 chain. This is the first report demonstrating that a laminin-like molecule from the salivary gland of O. fasciatus acts as a receptor for Phytomonas binding. The results presented in this investigation are important findings that will support further studies that aim at developing new approaches to prevent the transmission of Phytomonas species from insects to plants and vice-versa.

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Section: Discussionmentioning

confidence: 99%

Evidence That a Laminin-Like Insect Protein Mediates Early Events in the Interaction of a Phytoparasite with Its Vector's Salivary Gland

et al. 2012

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“…The proteolytic generation of kinin in tissues of T. cruzi-infected mice depends on chemokine secretion by macrophages activated by Toll-like receptors (353). The naturally occurring protease inhibitors play a role in cellular invasion by T. cruzi (346). Oligopeptidase B acting upon its substrate generates an agonist for host cell calcium release through adenylate cyclase and phospholipase C (51).…”

Section: Interactions Of Trypanosoma Cruzi With Vertebrate Hostsmentioning

confidence: 99%

“…Oligopeptidase B acting upon its substrate generates an agonist for host cell calcium release through adenylate cyclase and phospholipase C (51). The mitogen-activated protein kinase (MAPK) implicated in macrophage activity through gp83 signaling (440) favors the parasite invasion of the host cell (346).…”

Section: Interactions Of Trypanosoma Cruzi With Vertebrate Hostsmentioning

confidence: 99%

Pathogenesis of Chagas' Disease: Parasite Persistence and Autoimmunity

et al. 2011

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SUMMARY Acute Trypanosoma cruzi infections can be asymptomatic, but chronically infected individuals can die of Chagas' disease. The transfer of the parasite mitochondrial kinetoplast DNA (kDNA) minicircle to the genome of chagasic patients can explain the pathogenesis of the disease; in cases of Chagas' disease with evident cardiomyopathy, the kDNA minicircles integrate mainly into retrotransposons at several chromosomes, but the minicircles are also detected in coding regions of genes that regulate cell growth, differentiation, and immune responses. An accurate evaluation of the role played by the genotype alterations in the autoimmune rejection of self-tissues in Chagas' disease is achieved with the cross-kingdom chicken model system, which is refractory to T. cruzi infections. The inoculation of T. cruzi into embryonated eggs prior to incubation generates parasite-free chicks, which retain the kDNA minicircle sequence mainly in the macrochromosome coding genes. Crossbreeding transfers the kDNA mutations to the chicken progeny. The kDNA-mutated chickens develop severe cardiomyopathy in adult life and die of heart failure. The phenotyping of the lesions revealed that cytotoxic CD45, CD8 + γδ, and CD8α + T lymphocytes carry out the rejection of the chicken heart. These results suggest that the inflammatory cardiomyopathy of Chagas' disease is a genetically driven autoimmune disease.

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“…These include macrophages, epithelial and endothelial cells, fibroblasts, dendritic cells, neurites as well as cardiomyocytes (Meyer 1942, Meyer & Xavier de Oliveira 1948, Nogueira & Cohn 19��, Henriquez et al 1981, Meirelles et al 1982a, 198�, 1999, Morris et al 1988, Schenkman et al 1988, �raujo-Jorge 1989, OrtegaBarria & Pereira 1991, �prigliano et al 199�, Procópio et al 1998, Huang et al 1999, Chuenkova & PereiHuang et al 1999, Chuenkova & PereiChuenkova & Pereira 2001, Garzoni et al 200�, Melo et al 2004, Taniwaki et al 200�, Coimbra et al 200�, Bartholomeu et al 2008, Lu et al 2008, Poncini et al 2008, Scharfstein & Lima 2008). This single variable exemplifies the multitude of host cell and parasite components that, upon interaction, lead to activation of the signalling pathways discussed below.…”

Section: Discussionmentioning

confidence: 99%

“…No comparative data between both strains is evaluable for TCTs, but inhibitors of class I and class III PI�-K activities block the entry of the parasite into macrophages, suggesting the involvement of different isoforms of this kinase (Todorov et al 2000). On the other hand, it seems that calcium mobilisation from acidocalcisomes, but not from the ER, is important for cellular invasion by extracellular amastigotes of either the G or CL strains (Mor-Mortara et al 2005, Fernandes et al 200�, Scharfstein et al 200�, 2008, Scharfstein & Lima 2008.…”

Section: Signalling Mechanisms and Molecules Involved In T Cruzi Invmentioning

confidence: 99%

A century of research: what have we learned about the interaction of Trypanosoma cruzi with host cells?

Alves

Mortara

2009

Mem. Inst. Oswaldo Cruz

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Roles of Naturally Occurring Protease Inhibitors in the Modulation of Host Cell Signaling and Cellular Invasion by Trypanosoma cruzi

Cited by 25 publications

References 81 publications

Evidence That a Laminin-Like Insect Protein Mediates Early Events in the Interaction of a Phytoparasite with Its Vector's Salivary Gland

Evidence That a Laminin-Like Insect Protein Mediates Early Events in the Interaction of a Phytoparasite with Its Vector's Salivary Gland

Pathogenesis of Chagas' Disease: Parasite Persistence and Autoimmunity

A century of research: what have we learned about the interaction of Trypanosoma cruzi with host cells?

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