| Candida albicans |
Enterococcus spp. |
Synergy |
Germ-free and antibiotic-perturbed mice |
Enterococcal species are found to dominate the gastrointestinal microbiome following the introduction of C. albicans
|
[38] |
|
|
Antagonistic |
C. elegans coinfection model |
E. faecalis can inhibit C. albicans hyphal morphogenesis and virulence |
[38] |
|
C. albicans
|
Pseudomonas aeruginosa |
Antagonistic |
In vitro models |
P. aeruginosa lipopolysaccharide inhibits C. albicans biofilm and hyphal development |
[39] |
|
|
|
In vitro models |
P. aeruginosa excretes quorum-sensing molecules and quinolone signals, which repress hyphal and biofilm formation |
[39] |
|
|
|
In vitro models |
C. albicans secretes farnesol, which down-regulates the expression of P. aeruginosa virulence factors through modulation of the Pseudomonas quinolone signal system |
[39] |
|
|
|
In vitro models |
C. albicans inhibits the production of cytotoxic exotoxin A and pyoverdine |
[39] |
|
|
|
Neutropenic co-colonized mice |
Mice colonized with both P. aeruginosa and C. albicans had significantly lower mortality compared to those colonized with P. aeruginosa alone |
[39] |
|
C. albicans
|
Clostridium spp. |
Synergy |
In vitro models |
C. albicans coculture promotes C. difficile and C. perfringens growth in aerobic conditions |
[63] |
|
|
|
C. difficile mouse model |
Oral Candida administration worsens C. difficile severity |
[64] |
|
|
Antagonistic |
In vitro models |
p-cresol, produced by C. difficile, inhibits hyphal formation and virulence of C. albicans
|
[63] |
|
|
|
C. difficile mouse model |
C. albicans reduces C. difficile growth and C. difficile–related mortality, which appears dependent on the alterations that Candida induces on the gut bacteriome composition |
[40] |
