Increase in NF-kappaB binding affinity of the variant C allele of the toll-like receptor 9 -1237T/C polymorphism is associated with Helicobacter pylori-induced gastric disease.
We describe a unique, 4-generation pedigree with autosomal dominant gastropathy exhibiting the typical clinical, endoscopic, and pathological findings of Ménétrier-like disease, though in the absence of protein loss and with no increase in the levels of gastric TGF-α.
In the present study, real-time quantitative reverse transcription-polymerase chain reaction was used to analyze miR-421 levels in gastric juice from patients with gastric cancer or benign gastric disease, or normal.
Interestingly, mucin 5ac (muc5ac) gene expression in gastric corpus samples and gastric mucin production in stomach samples from the BF-1 group, but not the ST group, were significantly higher than those in the respective samples from the vehicle group.
Using high-throughput genotyping, the 24 tagSNPs were preliminarily assessed in a screening population of 552 controls, 254 GA and 236 GC subjects; subsequently, five candidate tagSNPs for gastric diseases risk in the TLR4, PGC and PTPN11 genes were re-evaluated in a larger population of 1276 controls, 907GA and 714 GC subjects.
In conclusion, our results suggest that the nonfunctional TLR1 602S/S genotype is associated with a reduced risk of H. pylori-induced gastric diseases, probably via diminished Th1 responses.
A frequent Toll-like receptor 1 gene polymorphism affects NK- and T-cell IFN-γ production and is associated with Helicobacter pylori-induced gastric disease.
Using high-throughput genotyping, the 24 tagSNPs were preliminarily assessed in a screening population of 552 controls, 254 GA and 236 GC subjects; subsequently, five candidate tagSNPs for gastric diseases risk in the TLR4, PGC and PTPN11 genes were re-evaluated in a larger population of 1276 controls, 907GA and 714 GC subjects.
Together, our results highlight inflammation-induced epigenetic silencing of miR-210 as a mechanism of induction of chronic gastric diseases, including cancer, during Hp infection.
Serum OPN levels increased from mild SG (1.99 ± 1.91 ng/ml) to AG (2.37 ± 2.27 ng/ml) to GC (5.94 ± 4.52 ng/ml) (P ≤ 0.002), along with increasing severity of gastric disease.
No association of polymorphisms at position +3954 of IL-1B and in the IL-1RN with H. pylori infection and with risk of severe gastric diseases was found.
Elucidation of the mechanism of gastrin modulation by HB-EGF-mediated EGF receptor transactivation should facilitate the development of therapeutic strategies against <i>H. pylori</i>-related hypergastrinemia and consequently gastric disease development, including gastric cancers.
Moreover, investigations in H. pylori-infected patients about polymorphisms of the genes encoding CXCL8 and inducible NO synthase, and epigenetic control of the ROS-producing enzyme spermine oxidase, have further proven that overproduction of these molecules impacts the severity of gastric diseases.