Table 2.
The interactions between C. albicans and bacteria.
| Trend | Bacteria | Year | Model | Major findings | Ref |
|---|---|---|---|---|---|
| Synergistic | Staphylococcus aureus | 2019 | Mice | S. aureus can strongly adhere to C. albicans hyphae. Such adhesion is mediated by the Als3p protein of C. albicans, thereby promoting disseminated S. aureus disease. | 119 |
| 2017 | In vitro | C. albicans fungal film supports the adhesion and colonization of S. aureus through close interaction with hyphal elements, forming a polymicrobial biofilm, and enhancing miconazole resistance. | 120 | ||
| Streptococcus gordonii | 2014 | In vitro | In addition to C. albicans’ Als3 and S. gordonii’ SspB mediating co-aggregation between fungal and bacterial cells, Als1 was also found to bind S. gordonii. | 121 | |
| 2009 | In vitro | S. gordonii AgI/II proteins (SspA and SspB) mediate adhesion to C. albicans. S. gordonii alleviates the inhibitory effect of the quorum-sensing molecule farnesol on C. albicans hyphae and biofilm production. | 122 | ||
| Antagonistic | Klebsiella pneumoniae | 2021 | Mice | C. albicans antagonizes K. pneumonia, whereas Staphylococcus spp. may antagonize Candida. | 123 |
| Enterococcus faecalis | 2019 | Mice | E. faecalis peptide EntV requires disulfide bond formation and is cleaved by proteases to produce peptides that inhibit C. albicans proliferation. | 124 | |
| 2017 | Mice | E. faecalis competes for overlapping niches by producing EntV, a 68 amino acid peptide that inhibits hyphal morphogenesis, biofilm formation, and virulence in C. albicans. | 125 | ||
| Lactobacilli | 2022 | In vitro | Lactobacillus johnsonii MT4 exhibits pH-dependent and pH-independent antagonistic interactions against C. albicans by acidifying the local environment and producing soluble metabolites, thereby inhibiting C. albicans planktonic growth and biofilm formation. | 126 | |
| 2022 | In vitro | Lactobacillus plantarum inhibits the growth of C. albicans and Streptococcus mutans and disrupts S. mutans-C. albicans cross-kingdom biofilms. | 127 | ||
| 2013 | Mice | Lactobacilli use endogenous tryptophan as a carbon source to amplify and produce the aryl hydrocarbon receptor (AhR) ligand, indole-3 aldehyde (3-IAld), which triggers the production of IL-22 in the gut. This results in colonization resistance to C. albicans and protection of the mucosa from inflammation. | 128 | ||
| Salmonella enterica serovar Typhimurium | 2011 | In vitro | Killing of C. albicans filaments by S. typhimurium is mediated by sopB effectors. | 129 | |
| Anaerobic bacteria | 2015 | Mice | They limit the proliferation of C. albicans by stimulating the production of intestinal mucosal immune defenses, particularly cathelicidin-related antimicrobial peptide (CRAMP). | 130 | |
| Streptococcus mutans | 2010 | In vitro | Mutanobactin A, a secondary metabolite of S. mutans, affects the transformation of C. albicans from yeast to mycelium. | 131 | |
| 2010 | In vitro | S. mutans secretes trans-2-decenoic acid, a diffusible signaling factor, that inhibits filamentation of C. albicans. | 132 | ||
| 2009 | In vitro | S. mutans production capacity-stimulating peptide (CSP) inhibits C. albicans embryo tube formation and yeast-to-hyphal transition. | 133 | ||
| Pseudomonas aeruginosa | 2013 | In vitro | The action of phenazine produced by P. aeruginosa inhibits C. albicans filamentation, intercellular adhesion, and biofilm development. | 134 | |
| 2004 | In vitro | Inhibition of C. albicans filamentous formation by secretion of 3-oxo-C12 homoserine lactone and induction of filamentous reversion to yeast morphology in a N-acetylglucosamine-containing medium. | 135 |
Ref: References