Shao Shihe
Jiangsu University, China
Posters & Accepted Abstracts: J Prob Health
Statement of the Problem: Helicobacter pylori (H.pylori) infection is closely with the human gastric mucosa-associated diseases. Recent several studies on miRNAs have expanded our insights on H.pylori pathogenesis. Findings: In this study, we found that miR-29a-3p was upregulated in H.pylori-positive gastric mucosa tissues and H.pyloriinfected gastric epithelial-derived cell lines. The upregulation of miR-29a-3p was dose dependent in BGC-823 and GES-1 cells infected with H.pylori.A20 (also known as tumor necrosis factor-�±-induced protein 3,TNFAIP3) is involved in NF-�ºB signaling pathway and cell proliferation. A20 was identified as target gene of miR-29a-3p.The expression of A20 was decreased in H.pylori-positive gastric mucosa tissues. A20 downregulation was time- and dose-dependent in gastric epithelial-derived cell lines infected with H.pylori. Conclusion & Significance: Overexpression of miR-29a-3p with miR-29a-3p mimic significantly blocked H.pylori-induced A20 expression, which suggests that H.pylori decreased A20 expression through upregulating miR-29a-3p in gastric epithelialderived cell lines infected with H.pylori. Functional findings showed that overexpression of A20 enhanced phosphorylated NF- �ºB p65 expression, promoted nuclear translocation of NF-�ºB p65 and the expression of inflammatory cytokines. Conversely, inhibition of A20 led to reduce the NF-�ºB p65 activation and the expression of inflammatory cytokines. In addition, compared to H.pyloriinfection group, IL-6 and IL-8 were decreased after silencing A20 and then infected H.pylori, which suggests silencing A20 can inhibit H.pylori induced inflammation. Together, the results suggest a new role of A20 in H.pylori infection and indicate it may positively regulate NF-�ºB activity and promote inflammation. The down expression of A20 may protect the body from damage in face of H.pylori infection.
