The human body is colonized by various microbes, among them the yeast . Mostly harmless, this opportunist causes also disease, ranging from superficial infections to sepsis. Risk factors are disturbed host defenses, mucosal barrier breakdown, and antibiotic-induced dysbiosis. Hence, residing bacteria are important to protect from Candida-mediated damage or inflammation. mpk, e.g., is described as positively immunomodulatory in mouse models of inflammatory bowel disease, but its effect on the mycobiota is unknown.

In this study we aimed to determine if mpk affects pathogenicity.

Therefore, intestinal and oral epithelial cellswere pre-infectedin vitrowith mpk and then challenged with SC5314. The role of soluble factors was investigated by spatial separation or use of Bacteroides-conditioned medium (BCM).

Preincubation of host cells with mpk strongly reduced -mediated damage while fungal burden and hyphal length were unaffected by the bacterium. The protective effect did not depend on direct contact of Bacteroidesto host cellsor and could be mimicked using BCM. Contact independency suggests that diffusible factors modulate host cell susceptibility.

Ongoing experiments aim to identifykey soluble Bacteroides mediators as well as subsequent host cell signaling. Additionally, co-colonization experiments of germ-free mice are planned to investigate mpk’s potential to mediate colonization resistance towards . This will contribute to our understanding of how commensal bacteria affect and host protection.

  • This is an open-access article distributed under the terms of the Creative Commons Attribution License.

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