Interleukin-6 Genetic Polymorphisms are not Related to Helicobacter pylori-Associated Gastroduodenal Diseases

Background. Polymorphisms in the promoter region of the proinflammatory cytokine, interleukin (IL)‐6 have been related to several chronic inflammatory diseases. Inter‐individual variation in the severity of gastric inflammation may be important in determining the clinical outcome of an Helicobacter...

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Veröffentlicht in:Helicobacter (Cambridge, Mass.) Mass.), 2003-04, Vol.8 (2), p.142-148
Hauptverfasser: Hwang, Il-Ran, Hsu, Ping-I., Peterson, Leif E., Gutierrez, Oscar, Kim, Jong G., Graham, David Y., Yamaoka, Yoshio
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Sprache:eng
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Zusammenfassung:Background. Polymorphisms in the promoter region of the proinflammatory cytokine, interleukin (IL)‐6 have been related to several chronic inflammatory diseases. Inter‐individual variation in the severity of gastric inflammation may be important in determining the clinical outcome of an Helicobacter pylori infection and relate to polymorphisms in this region. Materials and Methods. We studied H. pylori‐infected patients with duodenal ulcer or gastric cancer. In addition six gastric cancer cell lines, AGS, SNU‐668, MKN‐1, MKN‐7, MKN28 and KATOIII, were cocultured with both cag pathogenicity island‐positive and ‐negative H. pylori. Single nucleotide polymorphisms at positions −174, −572, and −597 in the IL‐6 promoter region were identified by PCR‐RFLP. The IL‐6 production from the cancer cells was determined by ELISA. Results. Sixty patients with gastric cancer and 60 with duodenal ulcer were studied. The alleles at positions −174 and −597 were closely linked (−174G/−597G or −174C/−597A) regardless of the ethnic group or disease presentation. There was no difference in the allele frequency at any of the sites among patient groups. H. pylori‐induced IL‐6 production from the gastric cancer cell lines was also independent of the IL‐6 polymorphisms or the presence of the cag pathogenicity island. Conclusions. The genetic polymorphisms in IL‐6 can be attributable to ethnicity and appear to be independent of the clinical outcome of an H. pylori infection.
ISSN:1083-4389
1523-5378
DOI:10.1046/j.1523-5378.2003.00135.x