Up‐regulation of cyclooxygenase‐1 and ‐2 in human gastric ulcer

Background: The expression of cyclooxygenase (COX) in human gastric ulcers is unknown. Aim: To study the expression and cellular localization of cyclooxygenase in human gastric ulcers. Methods: A total of 38 surgical gastric ulcer specimens were studied; 20 were Helicobacter pylori‐positive and 18 were associated with NSAID use. Twenty non‐ulcerated, histologically normal gastric specimens were used as controls. The cellular localization of COX‐1 and COX‐2 were determined by immunohistochemistry and double immunofluorescence. Cyclooxygenase messenger RNA (mRNA) was measured by reverse transcription‐polymerase chain reaction and localized by in situ hybridization. Results: In control specimens, COX‐1 was detected in stromal cells in the lamina propria. There was focal and weak immunostaining for COX‐2 in the foveolar epithelium. At the ulcer edge, COX‐1 was significantly increased in lamina propria cells whereas COX‐2 was strongly expressed in the hyperplastic foveolar epithelium in H. pylori‐ and non‐steroidal anti‐inflammatory drugs (NSAID)‐associated ulcers. At the ulcer base, there was strong expression of COX‐1 and COX‐2 in myofibroblasts, macrophages and endothelial cells in the granulation tissue, irrespective of H. pylori status or NSAID use. Messenger RNA of COX‐1 and COX‐2 were demonstrated by reverse transcription‐polymerase chain reaction. Double immunofluorescence and in situ hybridization confirmed the cellular localization of cyclooxygenase at protein and mRNA levels, respectively. Conclusion: Both COX‐1 and COX‐2 are up‐regulated in human gastric ulcers.