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Participation of the FFAR2 receptor in the inflammation in a DSS-induced colitis model

Grant number: 19/11662-0
Support type:Scholarships in Brazil - Master
Effective date (Start): July 01, 2019
Effective date (End): April 30, 2021
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal researcher:Marco Aurélio Ramirez Vinolo
Grantee:Sarah de Oliveira
Home Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated research grant:18/15313-8 - Investigation of the molecular mechanisms involved in the interaction between microbiota-derived metabolites and host cells during inflammation, AP.JP2


The gastrointestinal tract houses a diverse number of microorganisms, including bacteria, which are able to produce short chain fatty acids (SCFAs) through the fermentative metabolism of nondigestible carbohydrates from the diet. AGCCs are molecules that act on different biological functions, as well as act as signaling molecules that activate G protein-coupled receptors, such as FFAR2, such receptors are highly expressed in myeloid and epithelial cells. In neutrophils, the action of AGCCs may lead to their chemotaxis through FFAR2 receptor signaling. An imbalance of several factors can lead to inflammatory bowel diseases, among them colitis, an inflammatory condition that affects the intestinal colon. One of the experimental models used for colitis is induction by sodium dextran sulfate (DSS), where the action of the chemical compound leads to injury of the intestinal epithelial barrier and inflammation of adjacent tissue. Studies on the relationship of the FFAR2 receptor and intestinal inflammation with FFAR2 KO mice indicate that receptor activation in these cells plays an important role in the development of inflammatory diseases. However, the mechanisms behind this effect are not clearly defined once we have published conflicting results. In this context, the objective of this project is to identify the cellular participation of FFAR2 during intestinal inflammation caused by the administration of DSS. For this, we will use mice with deletion of this gene in the intestinal and neutrophil epithelial cells, in which colitis will be induced by the administration of DSS in the concentration of 2.5% in the drinking water. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
FACHI, J. L.; PRAL, L. P.; DOS SANTOS, J. A. C.; CODO, A. C.; DE OLIVEIRA, S.; FELIPE, J. S.; ZAMBOM, F. F. F.; CAMARA, N. O. S.; VIEIRA, P. M. M. M.; COLONNA, M.; et al. Hypoxia enhances ILC3 responses through HIF-1 alpha-dependent mechanism. MUCOSAL IMMUNOLOGY, v. 14, n. 4, . (18/15313-8, 15/15626-8, 18/22505-0, 19/11662-0, 19/06372-3, 17/16280-3, 17/06577-9, 18/02208-1)
Academic Publications
(References retrieved automatically from State of São Paulo Research Institutions)
OLIVEIRA, Sarah de. Analysis of the role of FFAR2 receptor in the inflammation in a DSS-induced colitis model. 2021. Master's Dissertation - Universidade Estadual de Campinas (UNICAMP). Instituto de Biologia Campinas, SP.

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