| Grant number: | 13/10905-0 |
| Support Opportunities: | Regular Research Grants |
| Start date: | April 01, 2014 |
| End date: | September 30, 2016 |
| Field of knowledge: | Health Sciences - Medicine - Surgery |
| Principal Investigator: | Alfredo Gragnani Filho |
| Grantee: | Alfredo Gragnani Filho |
| Host Institution: | Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil |
| City of the host institution: | São Paulo |
| Associated researchers: | LYDIA MASAKO FERREIRA ; Samuel Marcos Ribeiro de Noronha ; Sarita Mac Cornick ; Silvana Aparecida Alves Corrêa ; Veronica Chomiski Bicalho Custodio |
Abstract
Burns caused by various types of agents affect about one percent of the world population. More than a million burns occur in the U.S. each year and about 5000 of these injuries are fatal, causing the burn is the fourth leading cause of death from unintentional injuries in this country. The patients suffering burns have high susceptibility to infections and this is a concern with regard to the evolution and success of clinical treatment, being directly related to morbidity and mortality of the group. In order to prevent the entry and proliferation of the pathogenic organism has two types of immune response: the innate immunity (or natural) and acquired immunity (or specific). The immune response is responsible for the initial reactions to any infection and triggers the response of lymphocytes humoral and its products, which are components of acquired immunity, constituting a late response specific and long lasting. Burns produce changes in the pattern of immune response of the patient, represented both by stimulating the production of genes associated with the innate immune response and suppression of genes related to the adaptive immune response, especially those related to antigen presentation and activation of T lymphocytes. Thus, to evaluate the expression of genes related to innate and adaptive immunity as well as for wound healing in different cell types that make up the epidermis of burn patients becomes a key-point to better understand the molecular mechanisms underlying the response produced by epidermal stem cells. Moreover these cells are inserted in a microenvironment in which the types of cytokines and growth factors present there trigger one type of immune response that cannot be best suited to overcome the attack of microorganisms after burning. Moreover, it is also important to analyze the cytokines produced in the inter-play between cells involved in the healing process, especially those more differentiated, in this type of injury. Thus, we believe that this study can bring valuable information about burns and, thus, propose possible mechanisms to prevent the spread of infection in these patients. It is further emphasizing that, after extensive search of the literature no article on gene expression in skin cells, stem cell or not, in relation to the immune system (there are studies in blood cells) and the healing process where cells of the skin are fundamental. (AU)
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