AI-2 Induces Urease Expression Through Downregulation of Orphan Response Regulator HP1021 in Helicobacter pylori

Huang Yang; Xiaoxing Huang; Xiaochuan Zhang; Xiaoyan Zhang; Xiaohong Xu; Feifei She; Yancheng Wen

doi:10.3389/fmed.2022.790994

AI-2 Induces Urease Expression Through Downregulation of Orphan Response Regulator HP1021 in Helicobacter pylori

Front Med (Lausanne). 2022 Apr 1:9:790994. doi: 10.3389/fmed.2022.790994. eCollection 2022.

Authors

Huang Yang^{1

2}, Xiaoxing Huang^{1

2}, Xiaochuan Zhang^{1

2}, Xiaoyan Zhang^{1

2}, Xiaohong Xu^{1

2

3}, Feifei She^{1

2}, Yancheng Wen^{1

2}

Affiliations

¹ Key Laboratory of Gastrointestinal Cancer (Fujian Medical University), Ministry of Education, Fuzhou, China.
² Fujian Key Laboratory of Tumor Microbiology, Department of Medical Microbiology, Fujian Medical University, Fuzhou, China.
³ Fujian Medical University Union Hospital, Fuzhou, China.

Abstract

Helicobacter pylori causes gastric infections in more than half of the world's population. The bacterium's survival in the stomach is mediated by the abundant production of urease to enable acid acclimation. In this study, our transcriptomic analysis demonstrated that the expression of urease structural proteins, UreA and UreB, is induced by the autoinducer AI-2 in H. pylori. We also found that the orphan response regulator HP1021 is downregulated by AI-2, resulting in the induction of urease expression. HP1021 represses the expression of urease by directly binding to the promoter region of ureAB, ranging from -47 to +3 with respect to the transcriptional start site. The study findings suggest that quorum sensing via AI-2 enhances acid acclimation when bacterial density increases, and might enable bacterial dispersal to other sites when entering gastric acid.

Keywords: AI-2; HP1021; Helicobacter pylori; LuxS; quorum sensing; urease.