Helicobacter pylori (H. pylori) is a major etiologic agent causing chronic gastritis, along with other features, including lymphoid follicles, surface epithelial degeneration with mucous depletion and intestinal metaplasia. To clarify the mechanism by which H. pylori induces gastric mucosal injury and development of lymphoid follicles, in this study we examined the expression of the iNOS, cagA, CCL3 and CCLl8 mRNA in biopsy materials obtained from severe and mild chronic gastritis. Reverse transcription-PCR analysis showed that the rate of iNOS expression in mucosa of severe or mild chronic gastritis was 95.7% or 92.9, respectively. The expression of cagA mRNA in mucosa of severe chronic gastritis was 63.8%, but cagA mRNA was not found in mucosa of mild chronic gastritis. The expression of CCL3 mRNA in mucosa of severe chronic gastritis was 95.7%, but CCL3 mRNA was not found in mucosa of mild chronic gastritis. The expression of CCL18 mRNA was 53.2% in lymphoid follicle of gastric mucosa, but CCLl8 mRNA was found in gastric mucosa without lymphoid follicle (46.8%). The prevalence of expression of both cagA and CCL18 mRNA was 59.6% and cagA mRNA expression without CCLl8 was 16.7% in lymphoid follicle of gastric mucosa. These results suggest that the expression of iNOS mRNA in both mild and severe chronic gastritis is very high, therefore, the NO pathway is suspected of being an important factor in the etiology of chronic gastritis. The expression of cagA mRNA in gastric mucosa is associated with severity of chronic gastritis. Almost all of the CCLl8 mRNA positive gastric mucosa were also expressing cagA, therefore CCL18 mRNA expression is closely related to the cagA mRNA expression (p<0.0001).