Eicosanoids act in nodulation reactions to bacterial infections in newly emerged adult honey bees, Apis mellifera, but not in older foragers

Nodulation is the first, and qualitatively predominant. cellular defense re action to bacterial infections in insects. We tested the hypothesis that ei cosanoids also mediate nodulation reactions to bacterial challenge in adult s of a social insect, the honey bee, Apis mellifera. Treating newly-emerged experimental bees with the eicosanoid biosynthesis inhibitor, dexamethason e, impaired nodulation. reactions to bacterial infections, and the influenc e of dexamethasone was reversed by treating infected insects with arachidon ic acid, an eicosanoid precursor. Several other eicosanoid biosynthesis inh ibitors, including the cyclooxygenase inhibitor, indomethacin, and the dual cyclooxygenase/lipoxygenase inhibitor, phenidone, also impaired the abilit y of experimental honeybees to form nodules in reaction to bacterial challe nge. The influence of phenidone on nodulation was expressed in a dose-depen dent manner. However, in experiments with older honey bees foragers, simila r bacterial challenge did not evoke nodulation reactions. We infer from our results that while eicosanoids mediate cellular immune responses to bacter ial infections in newly emerged honey bees, and more broadly, in most insec t species, nodulation reactions to bacterial challenge probably do not occu r in all phases of insect life cycles. (C) 2001 Elsevier Science Inc. All r ights reserved.