Morphology |
CA yeast form preference in germ free mice. |
CA hyphal locked mutants show decreased virulence. |
GUT Morphology |
Specialized CA morphology that confers long-term GI fitness advantage. |
Unknown. |
Candidalysin |
CA mutants lacking candialys in have a colonization deficit in oral candidiasis model. Unknown phenotype in lower GI tract models. |
Unknown. |
Host Factors |
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Gut Microbiome |
Commensal anaerobic bacteria promote CA colonization resistance in mice. Lactobacillus spp. have been shown to decrease CA GI colonization levels in mice and humans. |
Commensal anaerobic bacteria probiotic therapy reduces CA dissemination in immunocompromised mice. |
Innate Immune Effector |
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Neutrophils |
No effect on CA GI colonization. |
Critical for preventing CA GI dissemination. |
Lymphocytes |
No effect on CA GI colonization. |
No effect on CA GI dissemination. |
Macrophages |
No effect on CA GI colonization. |
No effect on CA GI dissemination. |
NK cells |
No effect on CA GI colonization. |
No effect on CA GI dissemination. |
Pattern Recognition Receptors |
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Dectin-1 |
No effect on CA GI colonization. |
Critical for CA invasive disease phenotype. |
TLR2/4 |
Modulates CA GI colonization. |
Unknown. |
Environmental Factors |
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Medications |
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Antibiotics |
Antibiotics effective in depleting commensal anaerobic gut microbiota promote CA GI colonization. |
Increased GI CA burden resulting from antibiotics is associated with increased CA dissemination from the gut. |
Cancer chemotherapy |
Cancer chemotherapy induces changes in gut microbiota, but effects on CA GI colonization are unknown. |
Neutropenia and GI epithelial damage secondary to many cancer chemotherapies promote CA dissemination from the gut. |
Diet |
“Purified” mouse diets (which include corn syrup, sucrose, and soybean oil) promote CA GI colonization in mice, in the absence of antibiotics. |
Unknown. |