Protects Premature Intestinal Epithelial Cells from Invasion and Damage by .

is a leading cause of late-onset sepsis in premature infants and is thought to invade the host immature or damaged epithelial barriers. We previously showed that the hyphal form of invades and causes damage to premature intestinal epithelial cells (pIECs), whereas the non-hyphal , also a fungal pathogen of neonates, has less invasion and damage abilities. In this study, we investigated the potential for to modulate pathogenic interactions of with the premature intestine. While a mixed infection with two fungal pathogens may be expected to result in additive or synergistic damage to pIECs, we instead found that was able to protect pIECs from invasion and damage by . -induced pIEC damage was reduced to a similar extent by multiple different strains, but strains differed in their ability to inhibit invasion of pIECs, with the inhibitory activity correlating with their adhesiveness for and epithelial cells. cell-free culture fractions were also able to significantly reduce adhesion and damage to pIECs. Furthermore, coadministration of cell-free fractions with was associated with decreased infection and mortality in zebrafish. These results indicate that is able to reduce invasion, damage, and virulence functions of . Additionally, the results with cellular and cell-free fractions of yeast cultures suggest that inhibition of pathogenic interactions between and host cells by occurs secreted molecules as well as by physical contact with the cell surface. We propose that non-invasive commensals can be used to inhibit virulence features of pathogens and deserve further study as a non-pharmacological strategy to protect the fragile epithelial barriers of premature infants.