A relation histamine receptor and vascular permeability in the model of lung microvascular with endotoxemia.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24791956
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Emergency medicine
• Research Institution: Hyogo Medical University
• Principal Investigator: OSAKO TAKAAKI 兵庫医科大学, 医学部, 助教 (30573844)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ヒスタミン / 血管透過性 / 多価不飽和脂肪酸

Outline of Final Research Achievements

During acute lung inflammation, the lung microvasculature becomes hyperpermeable, resulting in immune cell infiltration and tissue edema. In this study, we examined the effects n-3 PUFAs onlung microvascular cell permeability.Human lung microvascular endothelial cells (HMVEC-L) were seeded on fibronectin-coated transwell inserts. The cells were pretreated with docosahexaenoic acid (DHA) or eicosapentaenoic acid (EPA) (n-3 PUFAS), and then treated with LPS to simulate acute lung injury. Pretreatment with DHA and EPA prior to LPS stimulation significantly attenuated LPS-induced cell permeability. EPA decreased histamine receptor 1 (H1R) and mRNA expression following LPS stimulation. Interleukin (IL)-6 mRNA expression in response to LPS treatment was significantly reduced by both DHA and EPA pretreatment. DHA and EPA attenuated LPS-induced lung microvascular endothelial cell permeability through a mechanism that may involve IL-6. EPA pretreatment may influence H1R expression.

Free Research Field

救急集中治療