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Introduction: During acute lung inflammation, the lung microvasculature becomes hyperpermeable, resulting in immune cell infiltration and tissue edema. N-3 polyunsaturated fatty acids (PUFAs), when used as a supplement in parenteral nutrition, can attenuate Lipopolysaccharide (LPS)-induced lung injury. In this study, we examined the effects n-3 PUFAs on lung microvascular cell permeability. Material and methods: 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 (1 μg/mL) to simulate acute lung injury. Microvascular permeability was assessed by monitoring the movement of FITCalbumin from the upper chamber to the lower chamber. The mRNA expression of tight junction proteins and regulators of adherens junctions were assessed by real-time PCR. VE-cadherin expression and localization was assessed by immune fluorescent staining. Results: Pretreatment with DHA and EPA prior to LPS stimulation significantly attenuated LPS-induced cell permeability. EPA decreased histamine receptor 1 (H1R) mRNA expression following LPS stimulation. Interleukin (IL)-6 mRNA expressions in response to LPS treatment was significantly reduced by both DHA and EPA pretreatment. Conclusions: 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.

Eicosapentaenoic Acid Decreases Histamine Receptor 1 Expression on Lung Microvascular Endothelial Cells and Cell Permeability during LPS Stimulation