Mice would coincide withFigure C. rodentium infection elicits colonocyte apoptosis to a higher degree in GC-C– mice than in GC-C++. A: Immunofluorescent detection from the apoptotic marker cleaved PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/17938273?dopt=Abstract caspase (CC) in representative sections of distal colon. PSI-7409 site elevated numbers of positively stained epithelial cells are visible in sections from mice at days and following infection in comparison to na e mice, with all the highest staining observed in GC-C– gut at day p.i. Scale bars m. B: A significant boost in the imply quantity of CC-positive intestinal epithelial cells (CC+ IEC) per higher energy field (HPF) was discovered in day p.i. distal colon of GC-C– compared to GC-C++ mice. Data is presented as the mean with SE. (P Student t test; Pna e vs. day p.i na e and day mice n per group; day mice n per group; D, day p.i D, day p.i.).elevated activation of pro-inflammatory genes. Relative to na e mice, we identified that there was increased liver expression of inflammatory cytokines and chemo-attractants including IL-, 
CXCL, and CXCL and that this improve was substantially far more in mice lacking GC-C (Figure). Similarly, lipopolysaccharide binding protein (LBP) was elevated at day p.i. in GC-C– liver. These data are consistent with initial barrier dysfunction occurring at day p.i. and suggests that intestinal barrier loss and circulation of luminal contents precedes translocation of reside bacteria in the gut lumen in these mice.Mann et al. BMC Gastroenterology , : http:biomedcentral-XPage ofAkD FITC-Dextran (ugml serum) ACFU g Liver NaiveDayNaiveDayGC-C++GC-C-GC-C–GC-C++GC-C–BGC-C++BGC-C++GC-C–ClaudinCGC-C++GC-C–ClaudinFigure Dissemination of C. rodentium in the intestine causes liver injury in GC-C– mice at day following infection. A: In colonized mice, GC-C– livers had drastically much more C. rodentium CFUg as in comparison with GC-C++ livers. (p). B: Gross regions of necrosis have been apparent inside the livers of some GC-C– mice at necropsy although none were observed in GC-C++ livers. C: Representative photomicrographs illustrate the presence of lymphocyte aggregates (black arrows) and regions of hemorrhage visible only in GC-C– mice (original magnification x).CClaudin Claudin TubulinGC-C++GC-C–Figure GC-C is essential to retain intestinal barrier function through C. rodentium infection. A: GC-C++ and GC-C– mice were provided a FITC-dextran tracer by oral gavage on day p.i. and serum fluorescence was measured 4 hours later. Relative to na e mice too as infected GC-C++ animals, GC-C– mice possess a substantial and considerable enhance in tracer movement from the gut lumen into the blood indicating a loss of intestinal barrier function. (P n mice per group). B: Immunofluorescent staining of claudin or claudin (green) with E-cadherin (red) and DAPI (blue) counter Biotin-VAD-FMK site stains reveals no apparent variations between infected manage and GC-C– mice at day p.i. C: Immunoblotting of claudin and claudin shows comparable protein levels in extracts from distal colon of mice infected by C. rodentium for days. Tubulin is shown to demonstrate equal loadingmensal microflora composition is altered in gut of na e mice lacking GC-CCommensal microflora load and diversity are strongly influenced by epithelial ion transport within the intestine-. Importantly, the pathogenicity of C. rodentium is impacted by the complement of commensal bacteria inside the gut ,. We for that reason used bacterial DNA extracted from stool to monitor any possible differences in bacterial load or composition in naive GC-C– mice c.Mice would coincide withFigure C. rodentium infection elicits colonocyte apoptosis to a greater degree in GC-C– mice than in 
GC-C++. A: Immunofluorescent detection on the apoptotic marker cleaved PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/17938273?dopt=Abstract caspase (CC) in representative sections of distal colon. Elevated numbers of positively stained epithelial cells are visible in sections from mice at days and following infection when compared with na e mice, with the highest staining seen in GC-C– gut at day p.i. Scale bars m. B: A significant enhance within the mean number of CC-positive intestinal epithelial cells (CC+ IEC) per higher energy field (HPF) was discovered in day p.i. distal colon of GC-C– in comparison to GC-C++ mice. Data is presented because the imply with SE. (P Student t test; Pna e vs. day p.i na e and day mice n per group; day mice n per group; D, day p.i D, day p.i.).elevated activation of pro-inflammatory genes. Relative to na e mice, we located that there was improved liver expression of inflammatory cytokines and chemo-attractants which include IL-, CXCL, and CXCL and that this boost was substantially additional in mice lacking GC-C (Figure). Similarly, lipopolysaccharide binding protein (LBP) was elevated at day p.i. in GC-C– liver. These data are constant with initial barrier dysfunction occurring at day p.i. and suggests that intestinal barrier loss and circulation of luminal contents precedes translocation of reside bacteria in the gut lumen in these mice.Mann et al. BMC Gastroenterology , : http:biomedcentral-XPage ofAkD FITC-Dextran (ugml serum) ACFU g Liver NaiveDayNaiveDayGC-C++GC-C-GC-C–GC-C++GC-C–BGC-C++BGC-C++GC-C–ClaudinCGC-C++GC-C–ClaudinFigure Dissemination of C. rodentium in the intestine causes liver injury in GC-C– mice at day following infection. A: In colonized mice, GC-C– livers had drastically far more C. rodentium CFUg as compared to GC-C++ livers. (p). B: Gross places of necrosis were apparent in the livers of some GC-C– mice at necropsy though none have been seen in GC-C++ livers. C: Representative photomicrographs illustrate the presence of lymphocyte aggregates (black arrows) and regions of hemorrhage visible only in GC-C– mice (original magnification x).CClaudin Claudin TubulinGC-C++GC-C–Figure GC-C is crucial to retain intestinal barrier function during C. rodentium infection. A: GC-C++ and GC-C– mice have been provided a FITC-dextran tracer by oral gavage on day p.i. and serum fluorescence was measured 4 hours later. Relative to na e mice too as infected GC-C++ animals, GC-C– mice have a substantial and substantial boost in tracer movement from the gut lumen into the blood indicating a loss of intestinal barrier function. (P n mice per group). B: Immunofluorescent staining of claudin or claudin (green) with E-cadherin (red) and DAPI (blue) counter stains reveals no apparent differences among infected handle and GC-C– mice at day p.i. C: Immunoblotting of claudin and claudin shows similar protein levels in extracts from distal colon of mice infected by C. rodentium for days. Tubulin is shown to demonstrate equal loadingmensal microflora composition is altered in gut of na e mice lacking GC-CCommensal microflora load and diversity are strongly influenced by epithelial ion transport inside the intestine-. Importantly, the pathogenicity of C. rodentium is impacted by the complement of commensal bacteria inside the gut ,. We therefore made use of bacterial DNA extracted from stool to monitor any possible differences in bacterial load or composition in naive GC-C– mice c.