• Helicobacter pylori
• non-steroidal anti-inflammatory drugs
• aspirin
• gastric mucosal injury
• neutrophils
• gerbils
• chronic pancreatitis
• SPINK1
• trypsin
• mutations
• PRSS1

Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs) cause the vast majority of peptic ulcers and their complications. However, their interaction remains extremely controversial. The study of Yoshida et al in this issue of Gut¹ aimed to address this issue by investigating the influence of experimental H pylori infection on gastric mucosal injury induced by aspirin in male Mongolian gerbils [see page 594].

The study found that aspirin caused more extensive haemorrhagic erosions associated with greater myeloperoxidase activity (an index of neutrophil accumulation), thiobarbituric acid reactive substance concentrations (an index of lipid peroxidation), and KC/GRO concentrations (a chemoattractive cytokine in rodents) in infected than in uninfected gerbils.

Furthermore, the authors repeated the experiments in gerbils pretreated with antineutrophil serum which reduced circulating neutrophils by 77%. Erosion index, myeloperoxidase activity, and thiobarbituric acid reactive substance concentration (but not KC/GRO concentration) were significantly less in such neutrophil depleted gerbils exposed to H pylori plus aspirin than in similarly exposed animals treated with control serum. Inhibitory effects on mucosal damage by antineutrophil serum administration was much greater in H pylori infected gerbils (65%) than in uninfected …