title: IL-1beta and IL-8, matrix metalloproteinase 3, and pepsinogen secretion before and after H. pylori eradication in gastroduodenal phenotypes.
abstract: OBJECTIVE
  Relations between host genetic factors and clinical outcomes of Helicobacter pylori infection are variable among ethnicities. The aim of this study was to examine gastric mucosal cytokines, matrix metalloproteinase 3 (MMP-3), and serum pepsinogen levels before and after eradication of H. pylori according to IL-1B genotypes and benign gastroduodenal phenotypes in a Korean population.
  
  
  METHODS
  A total of 349 Koreans including H. pylori-infected subjects (n=230) and H. pylori-negative controls (n=119) were enrolled. The former subjects were classified into groups according to the presence of non-atrophic gastritis (n=74), atrophic gastritis (n=56), gastric ulcer (n=37), and duodenal ulcer (n=63). IL-1B polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Gastric mucosal IL-1beta, IL-8, and MMP-3, and serum pepsinogen I and II levels were measured by ELISA and radioimmunoassay, respectively.
  
  
  RESULTS
  There were no significant differences between the IL-1B-31/-511 haplotype (TT/CC, CT/CT, and CC/TT) frequencies among the H. pylori-positive and -negative groups. The genotypes of IL-1B-31/-511 polymorphisms did not affect clinical phenotypes, inflammatory cytokines, MMP-3, and pepsinogen secretion. Subjects with H. pylori-infected atrophic gastritis exhibited significantly higher basal levels of cytokines and a lower pepsinogen I/II ratio than those of other groups. Following H. pylori eradication, inflammatory cytokines significantly decreased and the pepsinogen I/II ratio increased in all groups.
  
  
  CONCLUSIONS
  Mucosal inflammatory cytokines, MMP-3, and pepsinogen secretion are related to gastroduodenal phenotypes but not to IL-1B genotypes. Eradication of H. pylori can reduce mucosal inflammation and restore pepsinogen secretion.
authors.affiliation: Department of Gastroenterology, Kyung Hee University College of Medicine, Seoul, Korea.
authors.forename: Young Woon
authors.initials: YW
authors.lastname: Chang
authors.forename: Hyoung-Chul
authors.initials: HC
authors.lastname: Oh
authors.forename: Jae Young
authors.initials: JY
authors.lastname: Jang
authors.forename: Young
authors.initials: Y
authors.lastname: Hwangbo
authors.forename: Jae Won
authors.initials: JW
authors.lastname: Lee
authors.forename: Hyo Jung
authors.initials: HJ
authors.lastname: Lee
authors.forename: Kwang Ro
authors.initials: KR
authors.lastname: Joo
authors.forename: Seok Ho
authors.initials: SH
authors.lastname: Dong
authors.forename: Sung Soo
authors.initials: SS
authors.lastname: Kim
authors.forename: Hyo Jong
authors.initials: HJ
authors.lastname: Kim
authors.forename: Byung Ho
authors.initials: BH
authors.lastname: Kim
authors.forename: Rin
authors.initials: R
authors.lastname: Chang
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology*; D006239:Haplotypes; D016481:Helicobacter Infections / Q000188:drug therapy / Q000235:genetics*; D016480:Helicobacter pylori; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D007723:Korea; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000378:metabolism; D008875:Middle Aged; D020116:Pepsinogen A / Q000378:metabolism*; D010641:Phenotype; D011110:Polymorphism, Genetic
chemical_list: D053583:Interleukin-1beta; D016209:Interleukin-8; D020116:Pepsinogen A; D019278:Matrix Metalloproteinase 3