| Grant number: | 17/06444-9 |
| Support Opportunities: | Regular Research Grants |
| Start date: | February 01, 2018 |
| End date: | January 31, 2020 |
| Field of knowledge: | Health Sciences - Medicine |
| Principal Investigator: | Adriana Lino dos Santos Franco |
| Grantee: | Adriana Lino dos Santos Franco |
| Host Institution: | Universidade Nove de Julho (UNINOVE). Campus Vergueiro. São Paulo , SP, Brazil |
Abstract
The acute respiratory distress syndrome (ARDS) is characterized by endothelial rupture and alveolar injury due to an uncontrolled lung inflammatory response causing gas exchange impairment. Among the main causes of ARDS, sepsis is highlighted, especially in hospital settings. The restoration of normal lung function is very complicated and a phenomenon difficult to be studied; since the resolution of inflammation is a biochemically active process. Reduction of edema, clearance of neutrophils and repair of the alveolar barrier are prerequisites for the reestablishment of lung homeostasis. The mechanisms involved in this process in ARDS are little known and necessary for successful of therapy. Considering that ARDS is an important pathology with high mortality and that LED therapy is a promising treatment tool, our objective will be to evaluate the effect of LED therapy on the acute lung resolution process. For this, adult male Balb/c mice will be submitted to lipopolysaccharide (LPS, Salmonella abortus equi, ip) injection and irradiated or not with LED 1 and 5 h after the LPS injection. The analyzes will be performed 1, 3 and 5 days after LPS injection and will prioritize the neutrophil influx in the BAL, myeloperoxidase activity, evaluation of lung vascular permeability and edema, release and gene expression of inflammatory and pro-resolute mediators in the lung tissue, pulmonary function, evaluation of neutrophil apoptosis, macrophages phagocytosis, determination of T reg cells and, finally, evaluation of oxidative stress. Thus, we intend to study the effects of LED therapy on the resolution of lung inflammation. In this context, the proposed study may provide support for the understanding of the mechanisms that mediate ARDS, as well as allow proposing therapeutic alternatives for this important disease. (AU)
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