Serum levels of tumor necrosis factor-α, interleukin-6 and interleukin-8 are not increased in dyspeptic patients with Helicobacter pylori -associated gastritis

Author： Bayraktaroğlu Taner Şükrü Aras Ahmet Aydemir Selim Davutoğlu Can Üstündağ Yücel Atmaca Hulusi Borazan Ali

Publisher： Informa Healthcare

ISSN： 1466-1861

Source： Mediators of Inflammation, Vol.13, Iss.1, 2004-02, pp. : 25-28

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Abstract

Introduction : Helicobacter pylori ( H. pylori ) is a non-invasive microorganism causing intense gastric mucosal inflammatory and immune reaction. H. pylori- induced gastric mucosal cytokine overproduction has been clearly documented previously. The stomach has a large surface area and continuous spill-over of locally produced cytokines into the blood stream is a possibility. There are few and conflicting data on circulatory proinflammatory cytokine levels in patients with H. pylori infection. Materials and methods : Forty-two dyspeptic patients were enrolled into the study. The presence of H. pylori infection was diagnosed with antral histopathologic examination. After overnight fasting; serum samples were obtained from each patient to determine circulating interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) levels. Results : H. pylori was shown in 30 cases using Giemsa stain in antral histopathologic evaluation. Twelve cases were negative for H. pylori staining. Both the age and sex distribution had an insignificant difference in both H pylori -positive and H. pylori -negative groups. The mean circulatory levels of IL-6, IL-8 and TNF-a in both groups were not different. The situation was same in respect to the serum levels of these cytokines and the degree of inflammation, H. pylori density and activation scores according to Sydney classification. Conclusion : We could not show elevated circulatory levels of IL-6, IL-8 and TNF-α in H. pylori -infected cases. We believe that H. pylori -related cytokine activation become concentrated on gastric mucosa and this pathogen-induced local inflammatory cascade does not cause changes in circulatory levels of these cytokines. Moreover, there is no correlation between the levels of serum cytokines and Sydney parameters.