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MiRNA148a in immune response regulation of splenic leukocytes in Visceral Canine Leishmaniasis

Grant number: 19/04240-2
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): September 01, 2019
Effective date (End): July 31, 2021
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Valéria Marçal Felix de Lima
Grantee:Gabriela Torres Rebech
Home Institution: Faculdade de Medicina Veterinária (FMVA). Universidade Estadual Paulista (UNESP). Campus de Araçatuba. Araçatuba , SP, Brazil

Abstract

Leishmaniasis is a neglected disease caused by different species of protozoa of the genus Leishmania and affects several mammalian species, including humans. Associated with socio-economic and environmental factors, this disease is present in 98 countries, causing up to 1 million new cases and 30,000 fatal human victims per year. It was considered a rural disease, however, 70% of human cases have been occurring in urban areas in recent years being precedents of canine cases. In dogs, the immune response may vary between T1, characterized by the cellular response with the increase in the production of proinflammatory cytokines effective for the control of the parasite and, humoral type T2 response, with the production of anti-inflammatory cytokines that contribute to the progression of the disease. Suppression of the effective immune response directly affects host resistance and may be related to the expression of small RNA fragments called microRNAs (miRNAs) that alter the transcription of proteins and regulate various biological functions of the cells. The miRNA-148a has already been observed with increased expression in splenic leukocytes from dogs with Visceral Leishmaniasis. This miR can affect several pathways involved in regulating the immune response with altered expression of immune system proteins. Thus, the present study aims to evaluate the role of miR-148a in the production of TNF-±, IL-12, IL-6, IL-1beta, and PD1 in the transcription factors of T1/T2 responses using molecular tools to increase or decrease miR-148a. Our results could broaden the understanding of the disease aspect and generate knowledge for the development of therapeutic tools assisting in the treatment of the disease. (AU)