Immune system stimulation by the native gut microbiota of honey bees

It is now well known that “the human microbiome” (the bacteria that colonize the COLON, one’s large intestine) comprise 92% of all the DNA –– if a body becomes incinerated after death. Human DNA makes up the remaining 8%. And we know that the microbiomes of mice and other rodents are also very important in “health of that animal.”  Evolutionarily, going down the scale, how far can such a benefit of microbiomes be studied?  Well, it turns out the BEE has a microbiome that is important to its health.

Gut microbial communities can greatly affect host health –– by modulating the host’s immune system. For many important insects, however, the relationship between the gut microbiota and immune function remains poorly understood. In the attached article, authors test whether the gut microbial symbionts of the honey bee can induce expression of antimicrobial peptides, a crucial component of insect innate immunity.  Authors find that bees up-regulate gene expression of the antimicrobial peptides apidaecin and hymenoptaecin in gut tissue –– when the microbiota is present.

Using targeted proteomics, authors detected apidaecin in both the gut lumen and the haemolymph; higher apidaecin concentrations were found in bees harbouring the normal gut microbiota than in bees lacking gut microbiota.  In bacterial cell culture assays, cultured strains of the microbiota showed variable susceptibility to honey bee antimicrobial peptides –– although many seem to possess elevated resistance, compared with that in Escherichia coli.  In some trials, colonization by normal gut symbionts resulted in improved survivorship following injection with E. coli.  The authors’ results show that the native, non-pathogenic gut flora induces immune responses in the bee host.  Such responses (even in the lowly honey bee) appear to be a host mechanism to regulate the microbiota, and could potentially benefit host health by priming the immune system against future pathogenic infections.

R. Soc. Open Sci.  2o17; 4: 170003

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