n-3
polyunsaturated fatty acids (PUFA) influences a variety of disease conditions, such as
hypertension,
heart disease, diabetes,
cancer and allergic diseases, by modulating membrane constitution, inhibiting production of proinflammatory
eicosanoids and
cytokines, and binding to cell surface and
nuclear receptors. We have previously shown that
n-3 PUFA inhibit mast cell functions by disrupting high affinity
IgE receptor (FcεRI)
lipid raft partitioning and subsequent suppression of FcεRI signaling in mouse bone marrow-derived mast cells. However, it is still largely unknown how
n-3 PUFA modulate human mast cell function, which could be attributed to multiple mechanisms. Using a human mast cell line (
LAD2), we have shown similar modulating effects of
n-3 PUFA on FcεRI
lipid raft shuttling, FcεRI signaling, and mediator release after cell activation through FcεRI. We have further shown that these effects are at least partially associated with
ligation of
G protein-coupled receptor 120 expressed on
LAD2 cells. This observation has advanced our mechanistic knowledge of
n-3 PUFA's effect on mast cells and demonstrated the interplay between
n-3 PUFA,
lipid rafts, FcεRI, and
G protein-coupled receptor 120. Future research in this direction may present new targets for nutritional intervention and therapeutic agents.