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Role of chemerin in modulation of lung epithelial and endothelial cells in the comorbidity Asthma and Obesity

Grant number: 21/14343-3
Support type:Scholarships in Brazil - Doctorate (Direct)
Effective date (Start): July 01, 2022
Effective date (End): March 31, 2026
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal researcher:Vânia Luiza Deperon Bonato
Grantee:Núbia Sabrina Martins
Home Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:17/21629-5 - Strategies to study pulmonary inflammation during comorbidities, AP.TEM

Abstract

Obesity comprises a risk factor to Asthma exacerbation through neutrophilic inflammation, which characterizes a phenotype of severe Asthma. However, the mechanisms involved in exacerbation of lung inflammation in the comorbidity Asthma and Obesity is unknown. The adipokine chemerin is increase in the serum of obese patients and several works have demonstrate the role of chemerin in the inflammatory conditions. Although chemerin receptor is expressed by lung cells such as Airway Epithelial Cells (AEC) and Endothelial Cells (EC), the role of chemerin in lung inflammation is controversial with studies showing effects pro or anti-inflammatory of this adipokine. Both cells participate in the Asthma immunopathogenesis, AEC recognize the allergen and is essential to recruitment and activation of Dendritic Cells (DC) whereas activated EC produce endothelin-1 (ET-1), that induces an increase of mucus production and airway remodeling. In addition, EC also regulate the inflammatory processes through Endothelial Glycocalyx (EG), a network of proteoglycans and glycoproteins anchored in the membrane of the EC that controls the vascular permeability and leukocyte-endothelium interaction. Glycocalyx degradation results in increase of leukocytes transmigration to tissues, increasing the local inflammation. In this context, our hypothesis is that chemerin activates both, AEC and EC, contributing to DC, neutrophils and Th17 cells recruitment, as well promotes ET-1 production, resulting in increase of mucus production and tissue remodeling in the comorbidity Asthma and Obesity. We aim to search and identify target molecule and cells to promotes host-directed therapies in the context of comorbidity Asthma and Obesity. (AU)

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