Fig 11.

TLR2 is involved in the enhanced oral inflammatory response to C. albicans-streptococcal co-infection in vivo.A. Pro-inflammatory gene transcripts in tongue tissues of wild type and TLR2^−/− animals on day 5, as assessed by RT-qPCR. Results represent mean fold expression level of wild type over TLR2^−/− tissues, in 4 animals per group. Open bars: co-infection with C. albicans and S. oralis. Gray bars: C. albicans infection. *P < 0.01 and **P < 0.05 for a comparison between WT and TLR2^−/− expression levels.B. Immunofluorescence staining of frozen tongue sections (day 5) with monoclonal antibody NIMP-R14, highly specific for murine Ly-6G and Ly-6C. Neutrophils (red) are shown with white arrows. Note the relative absence of neutrophils adjacent to the mucosal biofilm. Bars = 50 μm.C. Comparison of MIP-2/CXCL2 protein concentration (pg g⁻¹ tissue) and MPO activity levels (U mg⁻¹ tissue) in tongue homogenates between WT (closed bars) and TLR2^−/− animals (open bars), co-infected with C. albicans and S. oralis. Mean of WT and TLR2^−/− tongue protein levels (8–12 animals per group) ± SEM, on day 5 post infection is shown. *P < 0.001, and **P < 0.05, compared with WT.D. Tongues from TLR2^−/− animals were homogenized, serially diluted and plated for C. albicans (Ca) or S. oralis (So) cfu counts on day 5. Similar to wild type animals (Fig. 12) co-infection increased oral colonization of S. oralis, but not C. albicans. Results of two independent mouse experiments, with 8–10 animals per group are shown. Bars indicate SEM. *P < 0.001 compared with single, S. oralis infection.