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Unraveling the molecular mechanisms underlying parasite-host interaction in Taenia solium Neurocysticercosis

Grant number: 20/04780-4
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): July 01, 2020
Effective date (End): June 30, 2022
Field of knowledge:Health Sciences - Medicine
Principal researcher:Iscia Teresinha Lopes Cendes
Grantee:Maria Carolina Pedro Athié
Home Institution: Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated research grant:13/07559-3 - BRAINN - The Brazilian Institute of Neuroscience and Neurotechnology, AP.CEPID


Parasite-host immune systems interactions results in a complex dance that evolved over millions of years. Learning its steps can help better understand the resulting disease, design viable effective treatments. A common parasitic cause of brain lesions is the infection by T. solium larvae or Neurocysticercosis (NCC). NCC is the most frequent parasitic disease in the human CNS. It is most prevalent in low and middle-income countries, where poor sanitation and free-roaming pigs are common. Unfortunately, it is not possible to explore the dynamics of immune response and inflammation throughout the course of NCC in human brain specimens since the brain tissue and the cysts are rarely removed by surgery. One way to overcome this problem is to use an animal brain models infected with the T. solium oncospheres such as rats (unnatural, brain innoculated T. solium oncospheres) and pigs (naturally infected). In these models, the combined use of RNA-Seq, laser-capture microdissection and single-cell separation and isolation should allow a more sensitive and precise analysis of the molecular mechanisms associated with the interactions between the parasite and the host's immune system. Our goal is to analyze how the transcriptome of a natural and unnatural host's brain (single-cells and tissue) adjacent to the cyst and the cysts transcriptome change over the course of infection, as well as identify changes in the hosts' immune response by identifying the celular profiles present in each time point. Knowing these mechanisms of inflammation and immune evasion should allow a better understanding of the crosstalk between the host's brain and the neurocysticercus over the course of the infection, and have a better insight about general or selected mechanisms of immune response. (AU)

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