Quality of ulcer healing in gastrointestinal tract: Its pathophysiology and clinical relevance

Figure 8 Original rat model of gastric ulcer recurrence. A: Ulcer scar of acetic-acid-induced gastric ulcer healed spontaneously (big arrow) with fold convergence (small arrows); B: Recurrence of ulcer with white coat at the same site as previous ulcer (big arrow). Interleukin-1β (IL-1β) or tumor necrosis factor α (TNF-α) administered systemically causes recurrence of ulcer macroscopically and histologically. Antineutrophil antiserum, antibodies against adhesion molecules, antibody against monocyte chemotactic protein-1 (MCP-1), or proton-pump inhibitors prevent recurrence. MCP-1 is overexpressed in macrophages in the interstitial space of the ulcer scar site at 12 h after administration of IL-1β or TNF-α. Adhesion molecules are overexpressed only at the ulcer scar site (Watanabe et al[22-24]). ICAM: Intercellular adhesion molecule.