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Objective .  CagA+/vacAs1+/vacAm1+ Helicobacter pylori  upregulates the expression of tumor necrosis factor receptor–associated factor 1 ( TRAF1 ), tumor necrosis factor receptor superfamily member 9 ( 4-1BB ), and B-cell lymphoma-extra large ( Bcl-xL ) in human gastric epithelial cells. We investigated the correlation between  cagA/vacAs1/vacAm1  and  TRAF1/4-1BB/Bcl-xL  expression in gastric mucosal tissue of patients with gastric disorders.  Methods . We collected gastric mucosa samples from 35 chronic, nonatrophic gastritis (CG) patients, 41 atrophic gastritis patients, 44 intestinal metaplasia with atypical hyperplasia (IM) patients, and 28 gastric carcinoma (Ca) patients. The expression of   TRAF1 ,  4-1BB , and  Bcl-xL  was determined using western blotting. The expression of  cagA, vacAs1 , and  vacAm1  in  H. pylori  was examined with polymerase chain reaction.  Results . The expression of  TRAF1 ,  4-1BB , and  Bcl-xL  was significantly upregulated in IM and Ca patients ( P  < 0.05 compared with CG). There were more cases of  cagA+/vacAs1+/vacAm1+ H. pylori  infection in samples with elevated  TRAF1 ,  4-1BB , or  Bcl-xL  expression ( P  < 0.05). Additionally, there were a remarkably large number of samples with upregulated  TRAF1/4-1BB/Bcl-xL  expression in cases of  cagA+/vacAs1+/vacAm1+ H. pylori  infection (44 cases, 67.7%;  P  < 0.05).  Conclusions . The pathogenesis of IM and Ca may be promoted by  cagA+/vacAs1+/vacAm1+ H. pylori , possibly via upregulated  TRAF1 ,  4-1BB , and  Bcl-xL  in gastric mucosal tissue.

Association between Virulence Factors andTRAF1/4-1BB/Bcl-xLExpression in Gastric Mucosa Infected withHelicobacter pylori