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. 2010 May 13;6(5):e1000902. doi: 10.1371/journal.ppat.1000902

Figure 5. Muc2 limits initial colonization of the mucosal epithelia, but ultimately controls levels of luminal pathogen burdens.

Figure 5

A. Fold differences of intimately adherent C. rodentium numbers present in the ceca of WT vs Muc2−/− mice 10 hours post-injection of 1.5×108 CFU into cecal lumen in a cecal loop surgery experiment (see Material & Methods). Results are of data from a total of 5 mice per group pooled from 2 individual experiments. Error bars  =  SEM (*P = 0.0109, Mann-Whitney test). B. Representative immunostaining for the C. rodentium-specific effector Tir in ceca acquired from cecal loop surgery, 10 hrs post-injection. C. rodentium is found on the surface of Muc2−/− cecal mucosa in a continuous fashion compared to WT mice, where Tir staining is patchy amid long stretches of uncolonized surface epithelium (white arrows). Original magnification, 100×. Scale bar  = 100 µm. C. Quantification of luminal C. rodentium vs. intimately adherent C. rodentium attached to the cecal and colonic mucosa in WT vs. Muc2−/− mice at 4 and 7 DPI. Results represent the mean value pooled from 2 independent infections containing 3–4 mice per group. Error bars  =  SEM (*P = 0.0140; **P = 0.005, Mann-Whitney test). D. Visualization of C. rodentium infection by staining for LPS (green) and Tir (red; red arrowhead), with nuclei specific DAPI (blue).as a counterstain. Tir staining is localized to the surface epithelium in both WT and Muc2−/− mice indicating direct infection, but the majority of LPS-positive cells in Muc2−/− mice are not infecting (Tir-negative), yet are accumulating on the surface of the mucosa. Original magnification, 200×. Scale bar  = 50 µm.