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Microb Pathog. 2019 Sep 9;137:103739. doi: 10.1016/j.micpath.2019.103739. [Epub ahead of print]

Investigation on the role of gene hp0788 in Helicobacter pylori in infecting gastric epithelial cells.

Author information

1
Department of Pathogenic Biology, School of Basic Medical Sciences, Binzhou Medical University, Yantai, China.
2
Department of Neurology, Second Hospital, Shandong University, Jinan, China.
3
School of Clinical Medicine, Binzhou Medical University, Yantai, China.
4
Department of Pathogenic Biology, School of Basic Medical Sciences, Binzhou Medical University, Yantai, China. Electronic address: sdboqingli@163.com.
5
Department of Pathogenic Biology, School of Basic Medical Sciences, Binzhou Medical University, Yantai, China. Electronic address: jxf_email@126.com.

Abstract

Helicobacter pylori infection can cause a wide range of digestive diseases. Gene hp0788 encodes an outer membrane protein HofF, which can reduce the bacterial adherence to the GES-1 cells and affect pathogenesis of H. pylori. In this study, the role of hp0788 in H. pylori infection was further analyzed. RNA-seq data showed that two genes (hp0523 and hp0539), located on the cagPAI, were down-regulated in Δ0788 mutant. The changes were confirmed through qRT-PCR, and the expression of these two genes will be almost recovered to the normal level in complemented strain. These two genes, hp0523 and hp0539, are known to be necessary for integrated T4SS, which related to CagA translocation and IL-8 induction. In H. pylori infected assay, lower amount of phosphorylated CagA and lower induction of IL-8 were both detected in GES-1 cells infected by Δ0788 mutant, compared with the wild type strain. Meanwhile, these reductions almost recovered to the wild-type level in complemented strain. These results reveal that there is a correlation between hp0788 disruption and CagA/IL-8 decline. Deletion of CagA-encoding gene (hp0547) in Δ0788 mutant was further constructed. The double deleted mutant shows lower IL-8-inducing capability than Δ0788 mutant, indicated the correlation between deficiency of CagA and reduced IL-8 production. These results together imply that disruption of hp0788 might affect the efficiency of T4SS and CagA injection, then weaken the induction of IL-8 in infected GES-1 cells.

KEYWORDS:

CagA; Gastric epithelial cells; Helicobacter pylori; IL-8; hp0788

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