Barrier Immune Effectors Are Maintained during Transition from Nurse to Forager in the Honey Bee

Abstract

Foragers facilitate horizontal pathogen transmission in honey bee colonies, yet their systemic immune function wanes during transition to this life stage. In general, the insect immune system can be categorized into mechanisms operating at both the barrier epithelial surfaces and at the systemic level. As proposed by the intergenerational transfer theory of aging, such immunosenescence may result from changes in group resource allocation. Yet, the relative influence of pathogen transmission and resource allocation on immune function in bees from different stages has not been examined in the context of barrier immunity. We find that expression levels of antimicrobial peptides (AMPs) in honey bee barrier epithelia of the digestive tract do not follow a life stage-dependent decrease. In addition, correlation of AMP transcript abundance with microbe levels reveals a number of microbe-associated changes in AMPs levels that are equivalent between nurses and foragers. These results favor a model in which barrier effectors are maintained in foragers as a first line of defense, while systemic immune effectors are dismantled to optimize hive-level resources. These findings have important implications for our understanding of immunosenescence in honey bees and other social insects.

Gut microbial communities of social bees

“…The cause of such perturbations is unclear. In honey bees, the immune responsiveness of gut epithelia was not found to be different between young nurse bees, which are confined to the hive, and older foragers, which encounter diverse microbes in the surrounding environment 71 , although this does not necessarily rule out community shifts due to nutritional or other stressors.…”

Non-Specific dsRNA-Mediated Antiviral Response in the Honey Bee

“…Previous investigations of honey bee immune responses have focused on immune responses to bacteria [22,62], fungi [63-69], a trypansomatid [69], and mites [70-72]. Investigation of honey bee antiviral responses has been hindered by lack of infectious honey bee virus clones, although some studies have been performed using semi-purified viruses and monitoring symptoms (reviewed in 6), colony size and weight [73], select gene expression [74], or antimicrobial peptide production in the context of either bacterial infection [75,76] or mite infestation [72]. RNAi-mediated antiviral immunity has been implicated [50-52,73], however honey bee antiviral defense mechanism(s) remain largely uncharacterized.…”

Negligible uptake and transfer of diet-derived pollen microRNAs in adult honey bees

“…To extend our previous research, we first collected honey bee nurses and forager as before 52 and examined the levels of MIR156a in both midgut and abdominal tissues. To verify our selection of nurses and foragers, we examined the levels of Vitellogenin (Vg) mRNA in the abdominal tissue of the collected bees and found decreased Vg expression in the abdomens of foragers (Fig.…”

“…When bees of specific life stage were required, nurses and foragers were collected from the same colonies at identical times using a mouth aspirator as before. 52 Newly eclosed bees were obtained by placing frames of emerging young bees from healthy colonies into an incubator (34 C, 60% relative humidity) overnight. For feeding experiments, bees returning to the hive without pollen loads were collected.…”