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pubmed:abstractText |
A striking example of immunosenescence is seen in the honey bee (Apis mellifera) worker caste. The bees' age-associated transition from hive duties to more risky foraging activities is linked to a dramatic decline in immunity. Explicitly, it has been shown that an increase in the juvenile hormone (JH) level, which accompanies onset of foraging behavior, induces extensive hemocyte death through nuclear pycnosis. Here, we demonstrate that foragers that are forced to revert to hive-tasks show reversal of immunosenescence, i.e. a recovery of immunity with age. This recovery, which is triggered by a social manipulation, is accompanied by a drop in the endogenous JH titer and an increase in the hemolymph vitellogenin level. Vitellogenin is a zinc binding glycolipoprotein that has been implicated in the regulation of honey bee immune integrity. We also establish that worker immunosenescence is mediated by apoptosis, corroborating that reversal of immunosenescence emerges through proliferation of new cells. The results presented here, consequently, reveal a unique flexibility in honey bee immunity--a regulatory plasticity that may be of general biological interest.
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pubmed:affiliation |
School of Life Sciences, Arizona State University, P.O. Box 874501, Tempe, AZ 85287, USA. gro.amdam@umb.no
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