This Month in Gastroenterology Laura Harrell, Eugene B. Chang  Gastroenterology  Volume 128, Issue 5, Pages 1153-1155 (May 2005) DOI: 10.1053/j.gastro.2005.03.062 Copyright © 2005 American Gastroenterological Association Terms and Conditions

Figure 1 (A) Capsule endoscopic appearance of small bowel with a mucosal break at 12 o’clock with surrounding erythema. (B) Capsule endoscopic appearance of a small bowel mucosal break associated with fresh hemorrhage. (C) Capsule endoscopic appearance of ileum with a large mucosal break. Gastroenterology 2005 128, 1153-1155DOI: (10.1053/j.gastro.2005.03.062) Copyright © 2005 American Gastroenterological Association Terms and Conditions

Figure 2 LT activity was measured by cytotoxicity of adrenal Y1 monolayers. As shown, cells were treated with 1:80 dilutions of unabsorbed LT extract, or with the same extract after absorption with CWG308 or CWG308:pLNT. Monolayers were photographed under phase-contrast microscopy (20×objective) after 24 hours of incubation. Note that pLNT blocks cytotoxicity of LT (right lower panel). Gastroenterology 2005 128, 1153-1155DOI: (10.1053/j.gastro.2005.03.062) Copyright © 2005 American Gastroenterological Association Terms and Conditions

Figure 3 IFN-γ treatment increases levels of ganglioside GM1 in Caco-2 cells, a component of lipid rafts. This figure shows dot blot analysis of Caco-2 cell lysates (2 μg and 5 μg protein) from either untreated cells or following exposure to IFNγ (100 IU/mL; 48 hours). Blots were incubated with a HRP-conjugate of the B subunit of cholera toxin to label GM1. Lysates from 2 separate control and IFN-treated cultures are shown. Gastroenterology 2005 128, 1153-1155DOI: (10.1053/j.gastro.2005.03.062) Copyright © 2005 American Gastroenterological Association Terms and Conditions

Figure 4 A schematic illustration of the proposed mechanism of toxin A-induced intestinal inflammation in the rat. A subtype of primary sensory neurons, with cell bodies in the dorsal root ganglia, express the TRPV1 receptor which can be stimulated directly by capsaicin and resiniferatoxin (RTX) and indirectly by toxin A via generation of leukotriene B4 (LTB4). TRPV1 stimulation results in substance P (SP) release orthodromically in the spinal cord in laminae I and II to contribute to the transmission of pain signals and antidromically in the intestine to cause inflammation. Capsazepine and iodo-resiniferatoxin (I-RTX) are TRPV1 antagonists that directly block TRPV1 activation by capsaicin, RTX, and LTB4, and indirectly block the LTB4-mediated effects of toxin A. Gastroenterology 2005 128, 1153-1155DOI: (10.1053/j.gastro.2005.03.062) Copyright © 2005 American Gastroenterological Association Terms and Conditions

Figure 5 Hierarchical cluster analysis using the 20 genes present in all 31 samples. Red denotes an increase and green a decrease when compared with the reference RNA pool. An asterisk denotes the patients who relapsed following treatment with IFN/rib. Note that normal liver tissue co-clusters with patients who respond to treatment, while all NR samples form part of a discrete cluster. Gastroenterology 2005 128, 1153-1155DOI: (10.1053/j.gastro.2005.03.062) Copyright © 2005 American Gastroenterological Association Terms and Conditions