| Summary: | The resistance of <i>Candida albicans</i> to conventional drug treatments, as well as the recurrence phenomena due to dysbiosis caused by antifungal treatments, have highlighted the need to implement new therapeutic methodologies. The antifungal potential of live biotherapeutic products (LBP) has already been demonstrated using preclinical models (cell cultures, laboratory animals). Understanding their mechanisms of action is strategic for the development of new therapeutics for humans. In this study, we investigated the curative anti-<i>C. albicans</i> properties of <i>Lactobacillus rhamnosus</i> Lcr35<sup>®</sup> using the in vitro Caco-2 cell and the in vivo <i>Caenorhabditis elegans</i> models. We showed that Lcr35<sup>®</sup> does inhibit neither the growth (<i>p</i> = 0.603) nor the biofilm formation (<i>p</i> = 0.869) of <i>C. albicans</i> in vitro. Lcr35<sup>®</sup> protects the animal from the fungal infection (+225% of survival, <i>p</i> < 2 × 10<sup>−16</sup>) even if the yeast is detectable in its intestine. In contrast, the Lcr35<sup>®</sup> cell-free supernatant does not appear to have any antipathogenic effect. At the mechanistic level, the DAF-16/Forkhead Box O transcription factor is activated by Lcr35<sup>®</sup> and genes of the p38 MAP Kinase signaling pathway and genes involved in the antifungal response are upregulated in presence of Lcr35<sup>®</sup> after <i>C. albicans</i> infection. These results suggest that the LBM strain acts by stimulating its host via DAF-16 and the p38 MAPK pathway.
|
|---|
