Cytokine expressions and H. pylori-associated gastric mucosal lesion.
To determine the role of host genetic factors in Helicobacter pylori infection, we examined the relation between gastroduodenal diseases and IL-1B polymorphisms in patients with H. pylori infection. In addition, we also compared gastric mucosal cytokine levels in those patients. We confirmed the findings that the IL-1B-31 C-to-T base transition was inverted in association with the -511 T-to-C base transition. There was no relation regarding to IL-1B polymorphisms and clinical outcomes. The gastric mucosal IL-1B level of the body of the stomach but not the antrum was significantly different among IL-1B genotypes. Furthermore, the IL-8 levels in the body were also higher in IL-1B-511C/C/ IL-1B-31TT than H. pylori negative patients. These findings suggested that IL-1B polymorphisms enhance not only IL-1-B production but also IL-8 production in the gastric body and may play an important role in the development of atrophic gastritis.
Takagi
Atsushi
A
Tokai University School of Medicine, Isehara, Kanagawa, Japan. takagia@is.icc.u-tokai.ac.jp
Deguchi
Ryuzo
R
Kobayashi
Kenji
K
Miwa
Takeshi
T
D016207:Cytokines / Q000096:biosynthesis*; D005753:Gastric Mucosa / Q000382:microbiology*; D005838:Genotype; D016481:Helicobacter Infections / Q000235:genetics / Q000382:microbiology; D016480:Helicobacter pylori / Q000378:metabolism* / Q000472:pathogenicity; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D011110:Polymorphism, Genetic; D013274:Stomach Neoplasms / Q000382:microbiology
D016207:Cytokines; D007375:Interleukin-1; D016209:Interleukin-8