Fig. S1.C. albicans promotes S. oralis colonization in the intestinal tract. DNA in stool samples of mice infected with C. albicans alone (Ca), S. oralis alone (So), or co-infected with C. albicans and S. oralis (CaSo) were analysed by qPCR using primers specific for the S. oralis gtfR gene.


Fig. S2. Mono-infection with S. oralis, at the same total microbial dose as co-infected animals, did not trigger mucosal inflammatory marker gene expression. Pro-inflammatory gene transcripts in tongue tissues of wild type animals on day 5 were assessed by RT-qPCR. Results represent mean fold expression level ± SD compared with uninfected, in 4 animals per group.


Fig. S3.S. oralis but not C. albicans activate pro-inflammatory signalling via TLR2. HEK-Blue™ -hTLR2 cells were challenged with live S. oralis 34 and/or C. albicans overnight and supernatants were analysed for alkaline phosphatase activity. Pam2CSK4 was used as a positive control. Two microbial cell doses were tested (Candida: 104, 105 cells ml−1, S. oralis: 105, 106 cells ml−1). HEK-Blue™ Null1 cells did not respond with alkaline phosphatase secretion to any stimulant (not shown). Error bars represent SD of triplicate experiments, *P < 0.001 compared with medium only.

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