Analysis of Toll-like receptor 2, 4, 6 and 9 genome DNA mutations in patients with tractable and intractable gastric mucosal diseases

Abstract

The possible involvement of Toll-like receptor (TLR) genome DNA in the prolongation and relapse of inflammatory intestinal diseases and alcoholic hepatic diseases has been reported. In this study, we examined the relationship of mutations of the TLR 2, 4, 6 and 9 genomic DNA to recurrent or intractable gastritis or gastric ulcers. The subjects were 32 patients, including 6 with H. pylori (Hp)-positive gastritis, 4 with Hp-negative gastritis, 10 with Hp-positive tractable gastric ulcer, 5 with Hp-positive recurrent gastric ulcer after Hp eradication, and 7 with Hp-negative easily recurrent gastric ulcer after Hp eradication. Gastric mucosal tissue and peripheral blood specimens were collected from each of the patients. DNA was extracted from the tissue and blood specimens and subjected to electrophoresis by the PCR method, using the oligonucleotide primers of TLR 2, 4, 6 and 9. The gastric mucosal tissue specimens were collected endoscopically from the sites of the lesions. Subsequently, the presence or absence of genomic DNA mutations in the blood and tissue specimens was examined using a DNA sequencer. TLR 2, 4, 6 or 9 DNA mutations were not observed in any of the gastric mucosal or peripheral blood specimens obtained from patients with tractable gastritis or gastric ulcer, or from those with intractable gastric ulcer who were Hp-positive or Hp-negative or had become Hp-negative after eradication therapy. These data suggest that mutations of the TLR 2, 4, 6 and 9 genome DNA may not be involved in the recurrence, delayed healing or intractability of gastritis and gastric ulcers.