Interleukin 1ß proinflammatory genotypes protect against gastro-oesophageal reflux disease through induction of corpus atrophy

T. Ando, Emad Munir El-Omar, Y. Goto, K. Nobata, O. Watanabe, O. Maeda, K. Ishiguro, M. Minami, N. Hamajima, H. Goto

Research output: Contribution to journalArticle

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Abstract

Background and aims: The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease ( GORD) is controversial but it is accepted that GORD is associated with increased exposure to gastric acidity. The proinflammatory interleukin ( IL)-1B polymorphisms increase the risk of hypochlorhydria and gastric atrophy. We examined the association between proinflammatory cytokine gene polymorphisms, presence of gastric atrophy, and risk of GORD in H pylori positive and negative subjects in Japan.

Methods: We studied 320 consecutive dyspeptic patients without peptic ulcers or cancers. GORD symptoms were scored using the Carlsson-Dent questionnaire and erosive oesophagitis was assessed endoscopically. H pylori infection was diagnosed by urea breath test, histological examination, and serology. Gastric atrophy was assessed histologically, and polymorphisms in the IL-1B, IL- 10, and tumour necrosis factor a ( TNF-A) genes were genotyped.

Results: Two hundred and eight patients were H pylori positive and 112 were negative. One hundred and eight ( 34%) were found to have erosive oesophagitis by endoscopic criteria ( grade A: 78; grade B: 23; grade C: 6; grade D: 1). Erosive oesophagitis and GORD symptoms were significantly more common in H pylori negative compared with H pylori positive subjects ( p < 0.05). H pylori positive subjects were more likely to have corpus gastric atrophy than H pylori negative subjects ( p < 0.001). Among H pylori positive patients, those without erosive oesophagitis or GORD symptoms were significantly more likely to have corpus atrophy than subjects with erosive oesophagitis or GORD symptoms ( p < 0.05). Among H pylori positive patients, subjects homozygous for the proinflammatory allele IL-1B-511T had a significantly lower risk of erosive oesophagitis ( odds ratio ( OR) 0.06 ( 95% confidence interval ( CI) 0.006 - 0.51); p = 0.01) and GORD symptoms ( OR 0.10 ( 95% CI 0.01 - 0.85); p = 0.04) compared with those homozygous for the -511C allele, while none of the two other proinflammatory cytokine gene polymorphisms had significant correlations with erosive oesophagitis or GORD symptoms.

Conclusions: A proinflammatory IL- 1B genotype is associated with increased risk of atrophy and decreased risk of GORD in H pylori infected subjects in Japan. These data indicate that in some genetically predisposed subjects, H pylori infection may protect against GORD through induction of gastric atrophy.

Original languageEnglish
Pages (from-to)158-164
Number of pages6
JournalGut
Volume55
Issue number2
DOIs
Publication statusPublished - Feb 2006

Keywords

  • HELICOBACTER-PYLORI INFECTION
  • CYTOKINE GENE POLYMORPHISMS
  • GASTRIC-CANCER
  • DUODENAL-ULCER
  • ACID-SECRETION
  • INCREASED RISK
  • ESOPHAGITIS
  • STRAINS
  • PREVALENCE
  • PATHOGENESIS

Cite this

Ando, T., El-Omar, E. M., Goto, Y., Nobata, K., Watanabe, O., Maeda, O., ... Goto, H. (2006). Interleukin 1ß proinflammatory genotypes protect against gastro-oesophageal reflux disease through induction of corpus atrophy. Gut, 55(2), 158-164. https://doi.org/10.1136/GUT.2005.072942

Interleukin 1ß proinflammatory genotypes protect against gastro-oesophageal reflux disease through induction of corpus atrophy. / Ando, T.; El-Omar, Emad Munir; Goto, Y.; Nobata, K.; Watanabe, O.; Maeda, O.; Ishiguro, K.; Minami, M.; Hamajima, N.; Goto, H.

In: Gut, Vol. 55, No. 2, 02.2006, p. 158-164.

Research output: Contribution to journalArticle

Ando, T, El-Omar, EM, Goto, Y, Nobata, K, Watanabe, O, Maeda, O, Ishiguro, K, Minami, M, Hamajima, N & Goto, H 2006, 'Interleukin 1ß proinflammatory genotypes protect against gastro-oesophageal reflux disease through induction of corpus atrophy' Gut, vol. 55, no. 2, pp. 158-164. https://doi.org/10.1136/GUT.2005.072942
Ando, T. ; El-Omar, Emad Munir ; Goto, Y. ; Nobata, K. ; Watanabe, O. ; Maeda, O. ; Ishiguro, K. ; Minami, M. ; Hamajima, N. ; Goto, H. / Interleukin 1ß proinflammatory genotypes protect against gastro-oesophageal reflux disease through induction of corpus atrophy. In: Gut. 2006 ; Vol. 55, No. 2. pp. 158-164.
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abstract = "Background and aims: The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease ( GORD) is controversial but it is accepted that GORD is associated with increased exposure to gastric acidity. The proinflammatory interleukin ( IL)-1B polymorphisms increase the risk of hypochlorhydria and gastric atrophy. We examined the association between proinflammatory cytokine gene polymorphisms, presence of gastric atrophy, and risk of GORD in H pylori positive and negative subjects in Japan.Methods: We studied 320 consecutive dyspeptic patients without peptic ulcers or cancers. GORD symptoms were scored using the Carlsson-Dent questionnaire and erosive oesophagitis was assessed endoscopically. H pylori infection was diagnosed by urea breath test, histological examination, and serology. Gastric atrophy was assessed histologically, and polymorphisms in the IL-1B, IL- 10, and tumour necrosis factor a ( TNF-A) genes were genotyped.Results: Two hundred and eight patients were H pylori positive and 112 were negative. One hundred and eight ( 34{\%}) were found to have erosive oesophagitis by endoscopic criteria ( grade A: 78; grade B: 23; grade C: 6; grade D: 1). Erosive oesophagitis and GORD symptoms were significantly more common in H pylori negative compared with H pylori positive subjects ( p < 0.05). H pylori positive subjects were more likely to have corpus gastric atrophy than H pylori negative subjects ( p < 0.001). Among H pylori positive patients, those without erosive oesophagitis or GORD symptoms were significantly more likely to have corpus atrophy than subjects with erosive oesophagitis or GORD symptoms ( p < 0.05). Among H pylori positive patients, subjects homozygous for the proinflammatory allele IL-1B-511T had a significantly lower risk of erosive oesophagitis ( odds ratio ( OR) 0.06 ( 95{\%} confidence interval ( CI) 0.006 - 0.51); p = 0.01) and GORD symptoms ( OR 0.10 ( 95{\%} CI 0.01 - 0.85); p = 0.04) compared with those homozygous for the -511C allele, while none of the two other proinflammatory cytokine gene polymorphisms had significant correlations with erosive oesophagitis or GORD symptoms.Conclusions: A proinflammatory IL- 1B genotype is associated with increased risk of atrophy and decreased risk of GORD in H pylori infected subjects in Japan. These data indicate that in some genetically predisposed subjects, H pylori infection may protect against GORD through induction of gastric atrophy.",
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author = "T. Ando and El-Omar, {Emad Munir} and Y. Goto and K. Nobata and O. Watanabe and O. Maeda and K. Ishiguro and M. Minami and N. Hamajima and H. Goto",
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TY - JOUR

T1 - Interleukin 1ß proinflammatory genotypes protect against gastro-oesophageal reflux disease through induction of corpus atrophy

AU - Ando, T.

AU - El-Omar, Emad Munir

AU - Goto, Y.

AU - Nobata, K.

AU - Watanabe, O.

AU - Maeda, O.

AU - Ishiguro, K.

AU - Minami, M.

AU - Hamajima, N.

AU - Goto, H.

PY - 2006/2

Y1 - 2006/2

N2 - Background and aims: The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease ( GORD) is controversial but it is accepted that GORD is associated with increased exposure to gastric acidity. The proinflammatory interleukin ( IL)-1B polymorphisms increase the risk of hypochlorhydria and gastric atrophy. We examined the association between proinflammatory cytokine gene polymorphisms, presence of gastric atrophy, and risk of GORD in H pylori positive and negative subjects in Japan.Methods: We studied 320 consecutive dyspeptic patients without peptic ulcers or cancers. GORD symptoms were scored using the Carlsson-Dent questionnaire and erosive oesophagitis was assessed endoscopically. H pylori infection was diagnosed by urea breath test, histological examination, and serology. Gastric atrophy was assessed histologically, and polymorphisms in the IL-1B, IL- 10, and tumour necrosis factor a ( TNF-A) genes were genotyped.Results: Two hundred and eight patients were H pylori positive and 112 were negative. One hundred and eight ( 34%) were found to have erosive oesophagitis by endoscopic criteria ( grade A: 78; grade B: 23; grade C: 6; grade D: 1). Erosive oesophagitis and GORD symptoms were significantly more common in H pylori negative compared with H pylori positive subjects ( p < 0.05). H pylori positive subjects were more likely to have corpus gastric atrophy than H pylori negative subjects ( p < 0.001). Among H pylori positive patients, those without erosive oesophagitis or GORD symptoms were significantly more likely to have corpus atrophy than subjects with erosive oesophagitis or GORD symptoms ( p < 0.05). Among H pylori positive patients, subjects homozygous for the proinflammatory allele IL-1B-511T had a significantly lower risk of erosive oesophagitis ( odds ratio ( OR) 0.06 ( 95% confidence interval ( CI) 0.006 - 0.51); p = 0.01) and GORD symptoms ( OR 0.10 ( 95% CI 0.01 - 0.85); p = 0.04) compared with those homozygous for the -511C allele, while none of the two other proinflammatory cytokine gene polymorphisms had significant correlations with erosive oesophagitis or GORD symptoms.Conclusions: A proinflammatory IL- 1B genotype is associated with increased risk of atrophy and decreased risk of GORD in H pylori infected subjects in Japan. These data indicate that in some genetically predisposed subjects, H pylori infection may protect against GORD through induction of gastric atrophy.

AB - Background and aims: The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease ( GORD) is controversial but it is accepted that GORD is associated with increased exposure to gastric acidity. The proinflammatory interleukin ( IL)-1B polymorphisms increase the risk of hypochlorhydria and gastric atrophy. We examined the association between proinflammatory cytokine gene polymorphisms, presence of gastric atrophy, and risk of GORD in H pylori positive and negative subjects in Japan.Methods: We studied 320 consecutive dyspeptic patients without peptic ulcers or cancers. GORD symptoms were scored using the Carlsson-Dent questionnaire and erosive oesophagitis was assessed endoscopically. H pylori infection was diagnosed by urea breath test, histological examination, and serology. Gastric atrophy was assessed histologically, and polymorphisms in the IL-1B, IL- 10, and tumour necrosis factor a ( TNF-A) genes were genotyped.Results: Two hundred and eight patients were H pylori positive and 112 were negative. One hundred and eight ( 34%) were found to have erosive oesophagitis by endoscopic criteria ( grade A: 78; grade B: 23; grade C: 6; grade D: 1). Erosive oesophagitis and GORD symptoms were significantly more common in H pylori negative compared with H pylori positive subjects ( p < 0.05). H pylori positive subjects were more likely to have corpus gastric atrophy than H pylori negative subjects ( p < 0.001). Among H pylori positive patients, those without erosive oesophagitis or GORD symptoms were significantly more likely to have corpus atrophy than subjects with erosive oesophagitis or GORD symptoms ( p < 0.05). Among H pylori positive patients, subjects homozygous for the proinflammatory allele IL-1B-511T had a significantly lower risk of erosive oesophagitis ( odds ratio ( OR) 0.06 ( 95% confidence interval ( CI) 0.006 - 0.51); p = 0.01) and GORD symptoms ( OR 0.10 ( 95% CI 0.01 - 0.85); p = 0.04) compared with those homozygous for the -511C allele, while none of the two other proinflammatory cytokine gene polymorphisms had significant correlations with erosive oesophagitis or GORD symptoms.Conclusions: A proinflammatory IL- 1B genotype is associated with increased risk of atrophy and decreased risk of GORD in H pylori infected subjects in Japan. These data indicate that in some genetically predisposed subjects, H pylori infection may protect against GORD through induction of gastric atrophy.

KW - HELICOBACTER-PYLORI INFECTION

KW - CYTOKINE GENE POLYMORPHISMS

KW - GASTRIC-CANCER

KW - DUODENAL-ULCER

KW - ACID-SECRETION

KW - INCREASED RISK

KW - ESOPHAGITIS

KW - STRAINS

KW - PREVALENCE

KW - PATHOGENESIS

U2 - 10.1136/GUT.2005.072942

DO - 10.1136/GUT.2005.072942

M3 - Article

VL - 55

SP - 158

EP - 164

JO - Gut

JF - Gut

SN - 0017-5749

IS - 2

ER -