Novel weapons: Invasive plant suppresses fungal mutualists in America but not in its native Europe

Why some invasive plant species transmogrify from weak competitors at home to strong competitors abroad remains one of the most elusive questions in ecology. Some evidence suggests that disproportionately high densities of some invaders are due to the release of biochemicals that are novel, and therefore harmful, to naive organisms in their new range. So far, such evidence has been restricted to the direct phytotoxic effects of plants on other plants. Here we found that one of North America's most aggressive invaders of undisturbed forest understories, Alliaria petiolata (garlic mustard) and a plant that inhibits mycorrhizal fungal mutualists of North American native plants, has far stronger inhibitory effects on mycorrhizas in invaded North American soils than on mycorrhizas in European soils where A. petiolata is native. This antifungal effect appears to be due to specific flavonoid fractions in A. petiolata extracts. Furthermore, we found that suppression of North American mycorrhizal fungi by A. petiolata corresponds with severe inhibition of North American plant species that rely on these fungi, whereas congeneric European plants are weakly affected. These results indicate that phytochemicals, benign to resistant mycorrhizal symbionts in the home range, may be lethal to naive native mutualists in the introduced range and indirectly suppress the plants that rely on them.

Biochanin A and prunetin improve epithelial barrier function in intestinal CaCo-2 cells via downregulation of ERK, NF-κB, and tyrosine phosphorylation

The single-layered gut epithelium represents the primary line of defense against environmental stressors; thereby monolayer integrity and tightness are essentially required to maintain gut health and function. To date only a few plant-derived phytochemicals have been described as affecting intestinal barrier function. We investigated the impact of 28 secondary plant compounds on the barrier function of intestinal epithelial CaCo-2/TC-7 cells via transepithelial electrical resistance (TEER) measurements. Apart from genistein, the compounds that had the biggest effect in the TEER measurements were biochanin A and prunetin. These isoflavones improved barrier tightness by 36 and 60%, respectively, compared to the untreated control. Furthermore, both isoflavones significantly attenuated TNFα-dependent barrier disruption, thereby maintaining a high barrier resistance comparable to nonstressed cells. In docking analyses exploring the putative interaction with the tyrosine kinase EGFR, these novel modulators of barrier tightness showed very similar values compared to the known tyrosine kinase inhibitor genistein. Both biochanin A and prunetin were also identified as potent reducers of NF-κB and ERK activation, zonula occludens 1 tyrosine phosphorylation, and metalloproteinase-mediated shedding activity, which may account for the barrier-improving ability of these isoflavones.