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. 2014 Aug 14;10(8):e1004257. doi: 10.1371/journal.ppat.1004257

Figure 1. C. albicans-induced epithelial cell signalling.

Figure 1

Oral epithelial cell discrimination of C. albicans yeast from hyphae is enabled via differential MAPK signalling. Recognition of yeast triggers activation of PI3K (green) and NF-κB (blue) as well as weak, transient activation of all three MAPK pathways (red). This MAPK activation leads to a transient activation of the c-Jun transcription factor via JNK/ERK1/2 signalling, with as-yet-unknown transcriptional effects. Activation of the PI3K pathway leads to activation of the epithelial damage protection and/or prevention response. Exposure of epithelial cells to C. albicans hyphae leads to the strong activation of MAPK signalling, resulting in the activation of the c-Fos transcription factor via the p38 pathway. At this point, regulation of MAPK signalling is initiated by the induction and stabilisation of the MAPK phosphatase, MKP1 (via the ERK1/2 pathway), which acts to regulate p38 and JNK signalling. Activation of c-Fos in the presence of NF-κB and PI3K signalling leads to the production of cytokines and inflammatory mediators, thereby activating immune responses to C. albicans.