Increased Mucosal Tumor Necrosis Factor-a and Interleukin-6 in Patients with Helicobacter pylori Infection.

1El-Metwally HAR , 2Salem OE and 3Baddour NM.

Departments of 1Medical Microbiology and Immunology, 2Internal Medicine and 3Pathology, Faculty of Medicine, Alexandria University.

To determine whether the inflammatory cytokines; TNF-a and IL-6 are implicated in the pathogenesis of Helicobacter pylori (H. pylori) associated gastroduodenal disease, the concentrations of  TNF-a and IL-6 in homogenate supernatants of gastric mucosal biopsy specimens from H. pylori positive and negative patients were measured by enzyme linked immunosorbent assay (ELISA). The study population comprised 50 patients with upper abdominal complaints, subjected to esophagogastroduodenscopy (EGD). Endoscopic diagnosis made as non erosive gastritis (G) and/or duodenitis (D), erosive (G) and/or (D), duodenal ulcer (DU) and patients without gastroduodenal lesion. Of these patients 28 (56%) were H. pylori positive; all had chronic gastritis by histopathological examination. The mucosal levels of TNF-a and IL-6 were significantly higher in H. pylori positive patients than in the negative patients (P< 0.001). The concentrations of TNF-a and IL-6 were higher in H. pylori positive patients with DU than in those with the non erosive G and/or D and erosive G and/or D. A significantly higher levels of  TNF-a was found in patients colonized by H. pylori with chronic active gastritis compared to chronic inactive gastritis and the mean was respectively 139.9 and 48.7 pg/mg protein (P< 0.001). In contrast, there was no significant difference in IL-6 production in patients with active or inactive gastritis. There was a significant correlation between IL-6 and TNF-a concentrations in H. pylori positive patients with active gastritis (r = 0.69 and P < 0.001). It is concluded that, inflammatory cytokines generated locally within the gastric mucosa could be relevant to the pathogenesis of H. pylori infection.