Echinacea purpurea microbiota: bacterial-fungal interactions and the interplay with host and non-host plant species in vitro dual culture.

Important evidence is reported on the antimicrobial and antagonistic properties of bacterial endophytes in Echinacea purpurea and their role in the modulation of plant synthesis of bioactive compounds. Here, endophytic fungi were isolated from E. purpurea, and the dual culture approach was applied to deepen insights into the complex plant-microbiome interaction network. In vitro experiments were carried out to evaluate the species specificity of the interaction between host (E. purpurea) and non-host (E. angustifolia and Nicotiana tabacum) plant tissues and bacterial or fungal endophytes isolated from living E. purpurea plants to test interactions between fungal and bacterial endophytes. A higher tropism towards plant tissue and growth was observed for both fungal and bacterial isolates compared to controls without plant tissue. The growth of all fungi was significantly inhibited by several bacterial strains that, in turn, were scarcely affected by the presence of fungi. Finally, E. purpurea endophytic bacteria were able to inhibit mycelial growth of the phytopathogen Botrytis cinerea. Bacteria and fungi living in symbiosis with wild Echinacea plants interact with each other and could represent a potential source of bioactive compounds and a biocontrol tool.

Phenotype-genotype relationships of SULT1A1 in human liver and variations in the IC50 of the SULT1A1 inhibitor quercetin.

Human sulfotransferases catalyze sulfate conjugation and 2 polymorphic genes, SULT1A1 and SULT1A2 in this family of transferases have been identified, encoding for 2 isoenzymes with very similar properties and substrate specificities. In order to test the hypothesis that variability in sulfation is due to genetic polymorphism in SULT1A1, the sulfation rate of 4-nitrophenol, a diagnostic substrate, was measured in 50 human liver samples and the genotype at the SULT1A1 locus was analyzed. The rate of 4-nitrophenol sulfation varied from 473 - 1,405 pmol/min/mg between the 5th and 95th percentiles, with a median and a mean +/- SD of 757 and 807 +/- 292 pmol/min/mg, respectively. The activities detected among the SULT1A1*2/*2 homozygotes (5 cases) were significantly lower than those of the other 2 genotypes, SULTA1*11/*1 and SULT1A1*1/*2 (5 and 40 cases, respectively), whereas there was no significant difference found between the SULT1A1*1/*1 and SULT1A1*1/*2 genotypes. To evaluate the possible influence of SULT1A2 polymorphism, genotype assays were also performed for this locus. No SULT1A2*2/*2 carrier, 26 SULT1A2*1/*1 and 24 SULT1A2*1/*2 were detected in the population sample under study. However, no correlation between the rate of 4-nitrophenol sulfation and the SULT1A2 genotype was detected. These results confirm that the variation in the rate of 4-nitrophenol sulfation in human liver is mainly due to SULT1A. Since SULT1A1*1/*2 polymorphism accounts for no more than 10% of the phenotypic variation seen in this cohort, other factors must also contribute to the variability in the rate of 4-nitrophenol sulfation in human liver. However, on the basis of the data obtained, variations in age, gender and liver function as possible causative factors can be excluded. The IC50 of quercetin, a potent inhibitor of 4-nitrophenol sulfation, was measured in the liver samples and ranged from 4.6 to 17.3 nM between the 5th and 95th percentiles. The median and the mean +/- SD were 7.7 nM and 8.3 +/- 2.5 nM, respectively. There was a weak but significant correlation between the IC50 value and age of the liver donors (r = 0.283, p = 0.046). The observed variation did not correlate with the genotypes at the SULT1A1 and SULT1A2 loci.