Study of vascular permeability in endothelial cells against Plasmodium berghei NK65

Malaria is a parasitic infectious disease considered a public health problem and represents a risk for the most diverse populations. Present in 104 countries, considered as endemic areas, this disease puts 40% of the world’s population at risk. Infections with Plasmodium spp. they can lead to a severe respiratory condition, with pulmonary complications called acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). This syndrome is characterized by acute inflammation, damage to the alveolar endothelium and pulmonary parenchyma, dysfunction and increased permeability of the pulmonary alveolar-capillary barrier and, consequently, edema formation. The large number of potentially involved factors, associated with great difficulties in the study of the disease in humans, makes the molecular basis of this pulmonary dysfunction still poorly understood, leading to high mortality in health units. Recent studies have shown that different components of the immune response are involved in the pathogenesis of ALI / ARDS associated with malaria and, both host and parasite factors, have important functions in the development of the disease. Murine models, used in LPA / ARDS research, have demonstrated the primordial involvement of neutrophils, various cytokines and chemokines in the process of increasing vascular permeability. The mechanisms for regulating the permeability of endothelial cells that involve dynamic interactions and structural changes in the components of the cytoskeleton play a critical role in modulating the inflammatory response and in maintaining the pulmonary endothelium. The future development of drugs that modulate this alveolar-capillary barrier may be essential to improve the prognosis of the disease.

Project details

Basic Science

Mar 2017 — Nov 2017

Brazil