No relationship between IL-1B gene polymorphism and gastric acid secretion in younger healthy volunteers.
OBJECTIVE
To investigate the influence of IL-1B-511 gene polymorphism on IL-1B mRNA expression and gastric acid output in individual with or without Helicobacter pylori (H pylori) infection.


METHODS
IL-1B mRNA expression and gastric acid secretion in 117 health volunteers were assayed using semi-quantitative RT-PCR and gastric juice assay, respectively. Pepsinogen (PG) I and II of 255 subjects (including 117 health volunteers) were also examined.


RESULTS
T/T genotype individuals with H pylori infection had a more decreased PG I/II ratio. In gastric antrum mucosa, the individuals with H pylori infection had higher IL-1B expression than those without H pylori infection, but there was no obvious difference among each genotype. In gastric corpus, the individuals with H pylori infection had a significantly higher IL-1B expression than those without H pylori infection. IL-1B-511T/T genotype was markedly higher as compared with the other two genotypes. Both maximal acid output and basic acid output were similar among each genotype in IL-1B-511 gene locus, regardless of H pylori infection.


CONCLUSIONS
IL-1B-511 T allele does not decrease gastric acid output, although it has a stimulated influence on IL-1B expression. Consequently, the pathway, through which IL-1B plays a central role in gastric cancer development, might not depend on low acid, but on the other regulation mechanisms.
Hu
Sheng
S
Institute of Cancer, the Cancer Hospital of Hubei Province, Wuhan 430079, Hubei Province, China. ehusmn@yahoo.com.cn
Song
Qi-Bing
QB
Yao
Ping-Fang
PF
Hu
Qing-Long
QL
Hu
Ping-Jin
PJ
Zeng
Zhi-Rong
ZR
Pang
Rui-Ping
RP
D000328:Adult; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D016481:Helicobacter Infections / Q000378:metabolism / Q000503:physiopathology*; D016480:Helicobacter pylori; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics*; D008297:Male; D011110:Polymorphism, Genetic; D013270:Stomach / Q000382:microbiology / Q000502:physiology*
D007375:Interleukin-1