Disruption of the <i>ECM33</i> Gene in <i>Candida albicans</i> Prevents Biofilm Formation, Engineered Human Oral Mucosa Tissue Damage and Gingival Cell Necrosis/Apoptosis

<table>Biofilm-forming ability of isogenic wild-type, <i>Caecm33</i> mutant, and revertant strains. (a) Metabolic activity of mature biofilms formed by the isogenic strains. (b–d) Fluorescence micrographs showing differences in morphology of biofilms formed by (b) wild-type, (c) <i>ECM33</i> mutant, or (d) revertant strain. RML1-heterozygous <i>Caecm33/CaECM33</i> mutant; RML2-homozygous <i>Caecm33</i> mutant; RML3-heterozygous <i>Caecm33/CaECM33</i> revertant; RML4-homozygous <i>ECM33/ECM33</i> revertant.</table>

Mediators of Inflammation

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Figure 1

Figure 1: Disruption of the <i>ECM33</i> Gene in <i>Candida albicans</i> Prevents Biofilm Formation, Engineered Human Oral Mucosa Tissue Damage and Gingival Cell Necrosis/Apoptosis 

Figure 1 | Disruption of the ECM33 Gene in Candida albicans Prevents Biofilm Formation, Engineered Human Oral Mucosa Tissue Damage and Gingival Cell Necrosis/Apoptosis 