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Comment
. 2016 Mar 16;3(5):191-195.
doi: 10.15698/mic2016.05.497.

The complexities of bacterial-fungal interactions in the mammalian gastrointestinal tract

Eduardo Lopez-Medina  1 , Andrew Y Koh  2
Affiliations
Comment

The complexities of bacterial-fungal interactions in the mammalian gastrointestinal tract

Eduardo Lopez-Medina et al. Microb Cell. .
No abstract available

Keywords: autophagy; cell death; differentiation; proliferation; starvation; trypanosome.

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Conflict of interest statement

Conflict of interest: The authors declare no conflict of interest.

Figures

Figure 1
Figure 1. Figure 1: Proposed mechanism of gut bacteria mediated Candida albicans gastrointestinal colonization resistance.
(A) Commensal gut bacteria, particularly obligate anaerobes (i.e. Bacteriodetes thetaiotamicron, Blautia producta), induce production of colonic host immune effectors, specifically antimicrobial peptides such as LL-37/CAMP which have Candicidal activity. (B) Bacterially derived fermentation products, short-chain fatty acids (SCFAs) may have a direct effect on C. albicans growth and colonization. (C) SCFAs can induce production of colonic antimicrobial peptides, including cathelicidins (LL-37/CAMP) and defensins that have activity against C. albicans.
Figure 2
Figure 2. 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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