Involvement of IL-17A in preventing the development of deep-seated candidiasis from oropharyngeal infection

In this study we show that Il17a-/- mice develop invasive candidiasis from oropharyngeal infection whereas WT mice do not. By using an established murine model of oral candidiasis we document the spatial and temporal progression of fungal infection. The histological analysis of tissues in Il17a-/- mice showed massive infiltration of the fungus in the stomach and alterations of the gastrointestinal tract segments. Both increased permeability and mucosal ulcerations of the intestinal barrier are seen to favour Candida albicans dissemination which was quantified both in kidney and liver where typical candidal abscesses were detected. Neutrophil from Il17a-/- were as capable of phagocytosing the fungus comparable to that of WT mice, however, they showed decreased candidacidal ability. Our data implies that IL-17A is crucial for preventing the passage from mucosal to disseminated candidiasis. As such, our model may be suitable to study the mechanisms favouring Candida albicans translocation to internal organs.