Anti-inflammatory effects of n–3 PUFA other than altered eicosanoid production
Although their action in antagonizing arachidonic acid metabolism is a key anti-inflammatory effect of n–3 PUFAs, these fatty acids have a number of other anti-inflammatory effects that might occur downstream of altered eicosanoid production or might be independent of this.
Cell culture studies demonstrate that EPA and DHA can inhibit the production of IL-1b and TNFa by monocytes  and the production of IL-6 and IL-8 by venous endothelial cells [30,31]. Fish oil feeding decreased ex vivo production of TNFa, IL-1b and IL-6 by rodent macrophages [32–34] and decreased the circulating concentrations of these cytokines in endotoxaemia . In some studies, supplementation of the diet of healthy human volunteers with fish oil has been reported to result in decreased production of TNF, IL-1 and IL-6 by mononuclear cells [10,12,36–40].
De Caterina et al.  showed that culture of human venous endothelial cells with DHA significantly decreased cytokine-induced surface expression of E-selectin, ICAM-1 (intercellular cell-adhesion molecule 1) and VCAM-1 (vascular cell adhesion molecule 1), and impaired the ability of ligand-bearing monocytes to adhere . EPA also inhibited LPS-induced expression of these three adhesion molecules on human venous endothelial cells, and again this had the functional effect of decreasing the binding of monocytes . Dietary fish oil decreased the expression of ICAM-1 on the surface of murine macrophages . Recently, dietary fish was found to decrease circulating levels of soluble VCAM-1 in elderly subjects , but it is not clear if this represents decreased surface expression of VCAM-1.