Figure 6
From: Subversion of human intestinal mucosa innate immunity by a Crohn’s disease-associated E. coli
Blockade of NFκB activation by AIEC LF82 induces massive epithelial apoptosis. Human normal colonic mucosa explant cultures were treated or not for 4 h with LF82 (109 bacteria per explant), with or without pretreatment with the NFκB nuclear translocation inhibitor SN50 (100 μg ml−1 for 40 min). (a) Hematoxylin-eosin (HE) standard staining, and immunoperoxidase staining with M30 and cleaved caspase-3 antibodies. In the presence of LF82, SN50 induces epithelial disruption and a massive increase in M30 and cleaved caspase-3-positive epithelial cells (brown cells; nuclei counterstained in blue). SN50 alone has no effect on crypt viability (right). (b) Quantitative evaluation of caspase-3-positive crypts (containing more than 30% positive epithelial cells) in LF82-infected explants in the presence or absence of SN50. Mean±s.e.m. of three independent experiments. (c) Immunoblot analysis of cleaved caspase-3 in lysates from LF82-treated explants with or without SN50. Representative of three independent experiments.
