Differential proteomics reveals novel insights into Nosema–honey bee interactions

Infection dynamics of Nosema ceranae in honey bee midgut and host cell apoptosis

“…In subsequent experiments, infected worker bees from this Nosema tolerant linage appeared to neither experience decreased rates of apoptosis (one form of PCD) (Kurze et al, 2015) nor energetic stress (Kurze et al, 2016b). A similar pattern was also found when comparing the midgut proteomes between infected workers of both the Nosema tolerant and a Nosema sensitive lineage (Kurze et al, 2016a).…”

“…As infestation appeared to increase from the anterior to the posterior epithelium at this relatively early stage of infection (Fries, 1988), our results strongly support previous suggestions that N. ceranae inhibits host cell apoptosis (Higes et al, 2013a;Kurze et al, 2015;Martin-Hernandez et al, 2017). An important role of PCD in bee-Nosema interactions was also indicated by proteomic and transcriptomic studies (Doublet et al, 2017;Dussaubat et al, 2012;Holt et al, 2013;Kurze et al, 2016a).…”

Deleterious Interaction Between Honeybees (Apis mellifera) and its Microsporidian Intracellular Parasite Nosema ceranae Was Mitigated by Administrating Either Endogenous or Allochthonous Gut Microbiota Strains

“…At the gene-expression level, honey bee midgut responded to N. ceranae infection by increasing oxidative stress pathway with the concurrent synthesis of antioxidant, defense, and protective molecules (Dussaubat et al, 2012;Di Pasquale et al, 2013). At the proteomic level, differential abundance of proteins associated to metabolism, response to oxidative stress, and apoptosis were measured between sensitive and resistant honey bees (Kurze et al, 2016). Other studies focused on other genetic mechanisms such as microRNA, which were suspected to regulate host honey bee metabolism related genes in response to N. ceranae infection (Huang et al, , 2016.…”

Honey Bee(Apis mellifera)Exposomes and Biological Pathways Associated withNosema ceranaeInfection

“…As Nosema infection is dependent on the host to supply ATP to reproduce 27 , it is not surprising that host metabolic pathways associated with carbohydrate metabolism are altered in response to infection. For example, changes in regulation of both gene expression and proteins such as alpha-glucosidase II, that are directly involved with carbohydrate catabolism and the generation of ATP through the electron transport chain, are consistently upregulated in previous studies 28,29,30 , and these changes may affect ubiquinone and terpene metabolism and differential expression of beta-tocopherol. We also observed differential expression of sulfur and dimethyl sulfone in this pathway.…”