Eicosanoid-regulated haemocyte motility mediates the inflammatory response in Mytilus edulis

In mussels, immunity relies on non-specific responses, mediated by haemocytes that leave circulation to infiltrate infected tissues and assault microbes. Whereas the main executive phase of immune defence, i.e. phagocytosis, is well documented, little is known about the first steps of inflammation and related regulation signals. Herein, we explored the involvement of arachidonic acid (AA)-eicosanoids signalling in cellular immune responses in vitro, using blockers of enzymes possibly involved and stimulators of inflammation. As glucocorticoids are anti-inflammatory steroids, we have exposed mussel haemocytes to dexamethasone, despite the lack of confirmation of corresponding cytosolic receptor expression in molluscs. Our dataset consolidates previous findings indicating that Mytilus edulis haemocytes in primary culture travel at 2.5 μm min^-1 1 h after plating, in acceleration over time, with a peak at 4.5 μm min^-1 after 24 h (15 °C). Hence, we consider that these cells are switched into an inflammatory state when placed in culture. Dexamethasone (100 μM) had no effect on phagocytosis nor ROS production but promoted cell detachment and inhibited migration. These effects were abolished by addition of AA (10 μM) and reproduced by specific inhibitors of cyclooxygenase or lipoxygenase. Treatment with PMA (0.01 μM, 0.1 μM and 1 μM) also resulted in a dose-dependent decrease of haemocyte velocity while exposure to the calcium ionophore A23187 (0.5 μM), dead bacteria or to their extracellular products speeded up migration. Altogether, our results indicate that M. edulis haemocyte motility is under control by the AA-eicosanoid pathway and that these cells are sensitive to chemokinetic substances altering cell migration.