Both in vitro studies and experiments in mice suggest a key role for transc
ription factor NF-kappa B as a mediator of mucosal inflammation. Experiment
s in vitro show that NF-kappa B activation may be a critical event in the p
roduction of proinflammatory molecules in Helicobacter pylori-associated ga
stritis, This study examines the expression and activity of NF-kappa B in s
itu in antral biopsies of 69 consecutive patients with immunohistochemical
techniques. In the uninflamed stomach, NF-kappa B was highly expressed and
active in a subset of epithelial cells, which were identified as predominan
tly G cells. In accordance with this activity, G cells were shown to expres
s high levels of the NF-kappa B target cytokine TNF-alpha, a well-documente
d stimulator of gastrin production. In patients with H. pylori-associated g
astritis, NF-kappa B activity was markedly enhanced. Activation occurred pr
eferentially in the epithelial cells. The number of cells showing activated
NF-kappa B correlated with the activity of gastritis, a measure of neutrop
hil influx, whereas no correlation was found with the chronicity of inflamm
ation, a measure of the presence of mononuclear inflammatory cells. This co
rrelation is direct evidence of the importance of NF-kappa B-dependent sign
al transduction for neutrophil influx in H, pylori-associated gastritis.