The synthesis and secretion of a variety of pro-inflammatory cytokines are increased in the chronic inflammatory reaction associated with Helicobacter pyloriinfection.1 In this issue (see page 24), Shibata and colleagues confirm increased secretion of tumour necrosis factor (TNF) by the inflamed mucosa, and provide evidence that duringH pylori infection there is both secretion of TNF and of the plasma membrane receptors for TNF, which are cleaved and secreted by gastric epithelial cells. Further experiments suggest that this secretion of soluble TNF receptors may be important in allowing the epithelial cell to protect itself from TNF induced death. Although there are relatively few normal controls in the human biopsy study, these results do suggest that the secretion of soluble TNF receptors may be an important defensive reaction, and may have implications for other inflammatory conditions of the gastrointestinal tract.

Since its discovery over 20 years ago, TNF has been recognised as an important mediator in the pathogenesis of a wide variety of diseases. TNF is one of family of related peptides, including Fas ligand and nerve growth factor, that acts through specific related cell surface associated receptors.2 The multiple biological …