dc.contributorUniversidade Federal de São Paulo (UNIFESP)
dc.creatorYoshida, Nobuko
dc.date.accessioned2015-06-14T13:41:01Z
dc.date.accessioned2019-05-24T16:49:43Z
dc.date.available2015-06-14T13:41:01Z
dc.date.available2019-05-24T16:49:43Z
dc.date.created2015-06-14T13:41:01Z
dc.date.issued2009-07-01
dc.identifierMemórias do Instituto Oswaldo Cruz. Instituto Oswaldo Cruz, Ministério da Saúde, v. 104, p. 101-107, 2009.
dc.identifier0074-0276
dc.identifierhttp://repositorio.unifesp.br/handle/11600/5135
dc.identifierS0074-02762009000900015.pdf
dc.identifierS0074-02762009000900015
dc.identifier10.1590/S0074-02762009000900015
dc.identifierWOS:000269123500014
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/2824387
dc.description.abstractFrequent reports on outbreaks of acute Chagas' disease by ingestion of food contaminated with parasites from triatomine insects illustrate the importance of this mode of transmission. Studies on oral Trypanosoma cruzi infection in mice have indicated that metacyclic trypomastigotes invade the gastric mucosal epithelium. A key molecule in this process is gp82, a stage-specific surface glycoprotein that binds to both gastric mucin and to target epithelial cells. By triggering Ca2+ signalling, gp82 promotes parasite internalisation. Gp82 is relatively resistant to peptic digestion at acidic pH, thus preserving the properties critical for oral infection. The infection process is also influenced by gp90, a metacyclic stage-specific molecule that negatively regulates the invasion process. T. cruzi strains expressing high gp90 levels invade cells poorly in vitro. However, their infectivity by oral route varies considerably due to varying susceptibilities of different gp90 isoforms to peptic digestion. Parasites expressing pepsin-susceptible gp90 become highly invasive against target cells upon contact with gastric juice. Such is the case of a T. cruzi isolate from an acute case of orally acquired Chagas' disease; the gp90 from this strain is extensively degraded upon short period of parasite permanence in the gastric milieu. If such an exacerbation of infectivity occurs in humans, it may be responsible for the severity of Chagas' disease reported in outbreaks of oral infection.
dc.languageeng
dc.publisherInstituto Oswaldo Cruz, Ministério da Saúde
dc.relationMemórias do Instituto Oswaldo Cruz
dc.rightsAcesso aberto
dc.subjectTrypanosoma cruzi
dc.subjectoral infection
dc.subjectmetacyclic trypomastigotes
dc.subjectsurface molecules
dc.subjectgp82
dc.subjectgp90
dc.titleMolecular mechanisms of Trypanosoma cruzi infection by oral route
dc.typeArtículos de revistas


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