FIGURE 2: Proposed mechanism of Candida albicans (CA) inhibition of Pseudomonas aeruginosa (PA) virulence in the gut. (A) PA gastrointestinal (GI) colonization. Despite inhibition of pyoverdine and pyochelin gene expression by CA, PA is able to colonize the murine GI tract, perhaps by utilizing alternative iron acquisition pathways (e.g. FeoABC system) that allow sustained growth and colonization of the gut. (B) CA-mediated Inhibition of PA Virulence. CA inhibits PA pyochelin and pyoverdine expression, most likely through a secreted protein. Production of PA extracellular virulence effectors, such as PrpL and exotoxin A, are decreased. Host gut epithelial integrity remains intact, and PA dissemination is prevented. (C) Iron-induced restoration of PA virulence. Iron supplementation in PA/CA co-colonized mice induces pyochelin-pyoverdine independent PA cytotoxic effector molecular production leading to increased gut permeability and mucosal barrier damage. PA can now disseminate from the gut.

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