An international team investigated cytokine secretion in subjects with chronic gastritis, and with or without Helicobacter pylori infection. Individuals with or without gastric cancer and gastric dysplasia were also assessed.
The researchers measured interleukin (IL)-8, IL-4, and interferon (IFN)-g in the tissue culture supernatant of gastric organ cultures from the subjects.
Interleukin-8 levels were found to be higher in cancer- and H. pylori-infected gastritis subjects than in H. pylori-negative subjects (mean 12.95, 10.48, and 4.49 ng/mL, respectively).
In gastric carcinoma, the near absence of mucosal IFN-g production may be critical in promoting growth of neoplastic cells.
|Dr Zhigang Ren
Elevated levels of IFN-g were detected in both H. pylori-infected and non-infected subjects with uncomplicated gastritis (72.23 and 34.61 pg/mL), and in non-infected dysplasia subjects (88 pg/mL).
Background levels of IL-4 (9.4 pg/mL or less) in uncomplicated gastritis subjects and relatively high levels of IL-4 in dysplasia subjects (25.8 pg/mL) were detected. In contrast, trace amounts of IFN-g (16.01 pg/mL) and high levels of IL-4 (42.81 pg/mL) in gastric biopsy culture supernatants were found in cancer subjects.
The researchers found that mucosal IL-4 levels correlated with infection and mucosal anti-H. pylori immunoglobulin G antibody. There was no such correlation with IL-8 levels.
Zhigang Ren, of the University of Newcastle, England, concluded on behalf of the group, "The significant differences between gastritis with and without cancer and dysplasia indicated a shift from a Th1 to a Th2 helper cell pattern of cytokine secretion.
"This study has identified a local mucosal defect in gastric cancer. The near absence of IFN-g production from the mucosa at the margins of the tumor may be a critical factor in promoting growth of neoplastic cells."