>
> #PLoS: Gut Pathology and Responses to the Microsporidium Nosema
> ceranae ... FULL PAPER May 2012
> http://dx.plos.org/10.1371/journal.pone.0037017
>
> Abstract Top
> The microsporidium Nosema ceranae is a newly prevalent parasite of the
> European honey bee (Apis mellifera). Although this parasite is
> presently spreading across the world into its novel host, the
> mechanisms by it which affects the bees and how bees respond are not
> well understood. We therefore performed an extensive characterization
> of the parasite effects at the molecular level by using genetic and
> biochemical tools. The transcriptome modifications at the midgut level
> were characterized seven days post-infection with tiling microarrays.
> Then we tested the bee midgut response to infection by measuring
> activity of antioxidant and detoxification enzymes (superoxide
> dismutases, glutathione peroxidases, glutathione reductase, and
> glutathione-S-transferase). At the gene-expression level, the bee
> midgut responded to N. ceranae infection by an increase in oxidative
> stress concurrent with the generation of antioxidant enzymes, defense
> and protective response specifically observed in the gut of mammals
> and insects. However, at the enzymatic level, the protective response
> was not confirmed, with only glutathione-S-transferase exhibiting a
> higher activity in infected bees. The oxidative stress was associated
> with a higher transcription of sugar transporter in the gut. Finally,
> a dramatic effect of the microsporidia infection was the inhibition of
> genes involved in the homeostasis and renewal of intestinal tissues
> (Wnt signaling pathway), a phenomenon that was confirmed at the
> histological level. This tissue degeneration and prevention of gut
> epithelium renewal may explain early bee death. In conclusion, our
> integrated approach not only gives new insights into the pathological
> effects of N. ceranae and the bee gut response, but also demonstrate
> that the honey bee gut is an interesting model system for studying
> host defense responses.

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