Actions of novel inflammation-resolving lipid mediators on human B cells (112.12)

Abstract

Abstract The resolution of inflammation is an active and dynamic process. Newly identified lipid mediators are now recognized as key players during the process of inflammation resolution. These lipid-derived molecules constitute four families of endogenous mediators (lipoxins, resolvins, protectins and maresins) derived from essential fatty acids. New findings also demonstrated that these lipid mediators regulate aspects of the immune response, including inhibition of neutrophil infiltration, reduction of T cell cytokine production and stimulation of macrophage phagocytic activity. Their actions on B lymphocytes are not known. Our results indicate that the lipoxin B4 and 17-HDHA, used at 100nM, increase the ability of normal human B cells to produce IgM and IgG when activated with CpG plus anti-IgM. The two lipid mediators also enhance B cell differentiation towards antibody secreting cells. In addition, resolvin D1 and aspirin-triggered resolvin increase antibody production in CpG-stimulated B cells. None of these inflammation resolution lipid mediators affect proliferation and are non-toxic to B cells. Increase of plasma cell differentiation and antibody production coincides with the known involvement of pro-resolving mediators during the late stages of inflammation and pathogen clearance.