Pap1 is an adhesin involved in the interaction of Sporothrix schenckii and Sporothrix brasiliensis with the host

<i>Sporothrix schenckii</i> and <i>Sporothrix brasiliensis</i> are causative agents of sporotrichosis, a mycosis that affects humans and other mammals. Adhesins are considered among the primary virulence factors of these species; however, their molecular identities are currently scarce. Here, we generated silenced mutant strains in <i>PAP1</i>, encoding a peptidorhamnomannan-associated protein, in both fungal species and compared their phenotypical characterization. <i>PAP1</i>-silenced mutants had normal growth, dimorphism, and morphology, suggesting the gene is not essential. The silenced strains showed defects in adhesion to HeLa cells, laminin, fibronectin, fibrinogen, type-I collagen, and type-II collagen. The <i>S. schenckii</i> silenced mutants showed a significant reduction in the adhesion to elastin, whilst the <i>S. brasiliensis</i> mutant showed impaired ability to bind thrombospondin 1 and to form biofilms. Both sets of <i>PAP1</i>-silenced mutants displayed defects in the cell wall composition, with reduced levels of cell wall rhamnose. The <i>S. schenckii</i> mutants showed a compensatory mechanism increasing cell wall mannose content, while the <i>S. brasiliensis</i> mutants increased cell wall protein levels in compensation to <i>PAP1</i> silencing. Both mutant sets changed their ability to stimulate cytokine production in human peripheral blood mononuclear cells and monocyte-derived macrophages. In addition, phagocytosis of <i>S. schenckii PAP1</i>-silenced strains was significantly increased, while the <i>S. brasiliensis PAP1</i>-silenced strains were poorly phagocytosed. Finally, <i>PAP1</i> silencing affected virulence in both species. These results suggest that <i>S. schenckii</i> and <i>S. brasiliensis PAP1</i> code for a protein with adhesive properties to different ligands. This is a cell wall protein that contributes to <i>Sporothrix</i> virulence and the interaction with immune cells.