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Contribution of IL-1 in the activation and function of ILC3 cells in the intestinal mucosa during obesity-induced metabolic syndrome

Grant number: 22/06787-1
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): September 01, 2022
Effective date (End): August 31, 2023
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Daniela Carlos Sartori
Grantee:Melissa Santana Gonsalez Machado
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

The change in the dietary patterns of the general population is characterized by the greater consumption of processed foods to the detriment of natural foods and dietary fiber, leading to an increase in the body fat index, which constitutes a risk factor for several chronic diseases, such as obesity, metabolic syndrome (MS) and type 2 diabetes mellitus. Excess weight leads to an increase in visceral adipose tissue and recruitment of immune system cells with a pro-inflammatory profile, leading to insulin resistance and MS. In this context, it was discovered that the intestinal microbiota undergoes changes in its composition (dysbiosis), leading to a plasma increase in molecular patterns associated with microorganisms (MAMPs), such as lipopolysaccharide (LPS). This process, called metabolic endotoxemia, occurs as a consequence of changes in the integrity of the intestinal barrier, due to the reduction of tight junctions. Innate type 3 lymphoid cells (ILC3) play a key role in the maintenance of the intestinal epithelium, as they are important producers of IL-22 and IL-17, which promote protection against bacterial infections, expression of junction proteins, mucins and antimicrobial peptides. . The production of these cytokines by ILC3 is stimulated by IL-1², via IL-1R, and IL-23. In this context, our group found a correlation between lower expression of IL-17 and IL-22 cytokines in the intestine (ileum) with high intestinal permeability during the progression of MS. Additionally, our group found that IL-1R-deficient mice developed more severe obesity and MS worsening and reduced IL-17 and IL-22 expression in the ileum, inferring the role of this IL-R1 receptor in the differentiation/activation of intestinal ILC3 and reduction in obesity-induced MS. Therefore, in this work, we will investigate the role of IL-1± or ² cytokines, via the IL-1R1 receptor, in the induction and function of ILC3 cells in intestinal homeostasis, as well as the improvement of metabolic and inflammatory changes associated with obesity and MS.

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