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Assessment of endothelial glycocalyx degradation in asthma and rhinovirus infection comorbidy

Grant number: 23/15628-7
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): March 01, 2024
Effective date (End): December 31, 2024
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Vânia Luiza Deperon Bonato
Grantee:Amanda Miranda França Zanel
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Rhinoviruses (RVs) is the main cause of the "common cold". However, RV infections also aggravate respiratory diseases, accounting for 80% of asthma exacerbations in children and 50% of episodes in adults. Although epidemiological data associates this viral infection with asthma crisis, the mechanisms by which the infection triggers these exacerbations have not yet been fully elucidated. Results from our group show that asthma promotes glycocalyx degradation and that obesity significantly increases glycocalyx deterioration in the pulmonary endothelium during asthma. The glycocalyx is a matrix that coats the luminal portion of the endothelium and is composed mainly of proteoglycans and glycoproteins anchored to the endothelial cell membrane. This structure acts to maintain leukocyte-endothelium interactions in order to regulate the overflow of these cell populations into adjacent tissues. In inflammatory conditions, degradation of the glycocalyx causes endothelial barrier dysfunction, increasing the inflammatory infiltrate and leading to tissue injury. The hypothesis of our project is that RV infection leads to glycocalyx degradation, increasing the recruitment of Th2 lymphocytes and eosinophils to the lungs, which is one of the mechanisms associated with the exacerbation of pulmonary inflammation in asthma. To test our hypothesis, we will use a comorbidity model of asthma induced by ovalbumin (OVA) followed by RV infection. The following experimental groups will be used as controls: CT group (control, no OVA, no RV), OVA group (experimental asthma only) and RV group (viral infection only). The production of inflammatory cytokines and the degradation of the endothelial glycocalyx will be assessed by measuring the components of this structure and by electron microscopy. The inflammatory profile resulting from the comorbidity of asthma and RV infection will also be analyzed. If our hypothesis is confirmed, we will have an association between the degradation of the glycocalyx of the pulmonary endothelium and the increased inflammatory response in the lungs in the comorbidity compared to asthma and RV infection, opening up perspectives for the study of glycocalyx constituents with immunomodulatory potential.

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