Pathogenesis of Helicobacter pylori (Hp) gastritis and duodenitis has not been fully explained yet. Aim of this project was to study topical duodenal and gastric cytokine production by means of ex-vivo in-vitro culture. A total number of 85 biopsy specimens were taken during routine gastroscopy from gastric and duodenal mucosa in 17 persons (6 men, 11 women,21–74 years old). Seven patients wereHppositive, 10 personsHpnegative. Biopsy specimens were cultured in vitro for 23 hours in the CO2 atmosphere at 37 °C. Cytokines were examined by means of sandwich enzymo-immuno-analysis in supernatant of previously homogenized cultured specimens, i.e. interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumour necrosis factor-α (TNF-α) and interleukin- 2 soluble receptor (sIL-2R). In group A (duodenal bulb), IL-1 negatively correlated with sIL-2R (r = -0.587; p = 0.035). In group B and C (gastric antrum), there was a significant correlation between IL-1 and IL-6 (r = 0.922, 0.631 resp.; p < 0.0001, 0.0208 resp.), IL-1 and TNFα (r = 0.921, 0.671 resp.; p = 0.0001, 0.0170 resp.), IL-6 and TNF-α (r = 0.7850; p = 0.0025). In group D (middle part of gastric corpus), there was a significant correlation between IL-1 and TNF-α (r = 0.710; p = 0.0097). In group E (gastric fundus), there was a significant correlation between IL-6 and IL-8 (r = 0.829; p = 0.0009). There was a borderline difference of IL-1 betweenHp positive and negative persons in group B (p = 0.051). IL-6 was higher in Hp positive patients in gastric fundus (p = 0.015) and middle antrum (p = 0.057). IL-8 was higher inHppositive subjects in middle antrum,but the differencewas not significant (p = 0.101). TNF-α in middle antrum was significantly higher in Hp positive individuals (p = 0.008). Host and microbes create a complex relationship in which microbes exert harmful (more often) or protective (less often) virtue. Their final effect is influenced by several factors including immunological condition of host, the treatment and the environment which all could modify bacterial phenotypic expression.

        Key words: Helicobacter pylori, ex vivo in vitro culture, interleukin-1β, interleukin-6, interleukin-8, tumour necrosis factor-α, interleukin-2 soluble receptor.