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Gut 1999;45:5-6; doi:10.1136/gut.45.1.5
Copyright © 1999 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 1999;45:5-6 ( July )

Commentary

See article on page 24

A key cytokine unlocks the door

The first 150 words of the full text of this article appear below.

The synthesis and secretion of a variety of pro-inflammatory cytokines are increased in the chronic inflammatory reaction associated with Helicobacter pylori infection.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 during H 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 . . . [Full text of this article]


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Relevant Article

Regulation of tumour necrosis factor (TNF) induced apoptosis by soluble TNF receptors in Helicobacter pylori infection
J Shibata, H Goto, T Arisawa, Y Niwa, T Hayakawa, A Nakayama, and N Mori
Gut 1999 45: 24-31. [Abstract] [Full Text] [PDF]

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