Premium
Noradrenaline reduces the stimulatory effect of interleukin‐1α on reactive oxygen species production by oyster immunocytes
Author(s) -
Lacoste Arnaud,
Malham Shelagh K.,
Cueff Anne,
Poulet Serge A.
Publication year - 2001
Publication title -
invertebrate biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.486
H-Index - 42
eISSN - 1744-7410
pISSN - 1077-8306
DOI - 10.1111/j.1744-7410.2001.tb00043.x
Subject(s) - rolipram , biology , stimulation , agonist , receptor , autocrine signalling , signal transduction , microbiology and biotechnology , reactive oxygen species , medicine , endocrinology , phosphodiesterase , biochemistry , enzyme
. A growing body of evidence suggests that interleukin‐1α (IL‐1α) is present in invertebrates. Both invertebrate and human IL‐1α can bind to invertebrate receptors and stimulate invertebrate immune functions. The present study shows that IL‐1α increases reactive oxygen species (ROS) production by oyster immunocytes. However, physiological doses of noradrenaline (NA) exert a suppressive effect on IL‐1α stimulation in vitro . The β‐adrenoceptor agonist isoproterenol mimicked the effects of NA and the β‐adrenoceptor antagonist propanolol blocked the NA‐induced suppression of hemocyte responsiveness to IL‐1α. The type IV phosphodiesterase inhibitor rolipram acted in synergy with isoproterenol to reduce hemocyte response to IL‐1α and the protein kinase A inhibitor H‐89 suppressed the effects of isoproterenol. These results suggest that circulating NA impairs IL‐1α‐stimulation of oyster hemocyte via a β‐adrenoceptor/cyclic AMP/protein kinase‐A signaling pathway. Considering that mollusc immunocytes secrete NA, an autocrine regulatory loop may also modulate the ability of these cells to respond to IL‐1α.