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Figure 7 | Cell Communication and Signaling

Figure 7

From: The Campylobacter jejuniCiaD effector protein activates MAP kinase signaling pathways and is required for the development of disease

Figure 7

CiaD is required for the development of severe disease. (A) Gross pathology of IL-10-/- mice infected with C. jejuni. Significant differences in gross pathology were observed between the C. jejuni wild-type strain and the ciaD mutant. The C. jejuni ciaD complemented isolate partially restored the gross pathology to levels intermediate between the C. jejuni wild-type strain and ciaD mutant. (B) Ileocecocolic histopathologic lesion scores of all mice in the in vivo oral challenge study. Lesion scores for the ciaD mutant group and the C. jejuni wild-type group were significantly different, based on nonparametric Kruskal Wallis one-way ANOVA followed by the Mann–Whitney test for pairwise comparisons and the Holm-Šidák procedure for correction for multiple comparisons. Lesion scores in the ciaD complemented group showed that 3/13 (23%) of mice had restoration of the inflammatory phenotype. One mouse in the trypticase soy broth (TSB) treated group had spontaneous colitis. (C) Representative histopathology of ileocecocolic junctions. Bars represent 100 μm. Treatment groups were as follows: (1) mouse sham inoculated with trypticase soy broth, (2) mouse infected with the C. jejuni wild-type strain 11168, (3) mouse infected with the ciaD mutant, and (4) mouse infected with the ciaD complemented isolate. Note that the knockout of ciaD prevented tissue inflammation (panel 3) with tissues appearing similar to the TSB controls (panel 1); brackets in panels 1 and 3 show the normal crypt height. Mice receiving the C. jejuni wild-type strain (panel 2) had severe end stage typhlocolitis with significant increases in the crypt height of the lamina propria (upper bracket) and submucosa due to edema (lower bracket). Mononuclear cell infiltrates (dark purple cells) can be seen throughout the tissue. Complementation with ciaD restored the phenotype to that of severe typhlocolitis in the mouse shown in panel 4.

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