Clarithromycin resistance and 23S rRNA gene mutation characteristics of <i>Helicobacter pylori</i> isolates from patients in Qiannan Autonomous Prefecture

Qi, Ting-Na; Pan, Ke; Wang, Fei; Wei, Gang; Jiang, Yideng; Zhang, Ren-Hong; Zheng, Juan; Zhang, Dandan; Chen, Zhenghong

doi:10.11569/wcjd.v23.i18.2901

Cited by 2 publications

(1 citation statement)

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“…For resistant strains, PCR amplification of the 23S rRNA and sequence analysis were performed to examine the genetic basis of these resistant phenotypes. The above-described experiment details have been previously reported in a published article ( 53 ).…”

Section: Methodsmentioning

confidence: 99%

The Bifunctional Enzyme SpoT Is Involved in the Clarithromycin Tolerance of Helicobacter pylori by Upregulating the Transporters HP0939, HP1017, HP0497, and HP0471

Geng

Chen

et al. 2017

Antimicrob Agents Chemother

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Clarithromycin (CLA) is a commonly recommended drug for Helicobacter pylori eradication. However, the prevalence of CLA-resistant H. pylori is increasing. Although point mutations in the 23S rRNA are key factors for CLA resistance, other factors, including efflux pumps and regulation genes, are also involved in the resistance of H. pylori to CLA. Guanosine 3′-diphosphate 5′-triphosphate and guanosine 3′,5′-bispyrophosphate [(p)ppGpp)], which are synthesized by the bifunctional enzyme SpoT in H. pylori, play an important role for some bacteria to adapt to antibiotic pressure. Nevertheless, no related research involving H. pylori has been reported. In addition, transporters have been found to be related to bacterial drug resistance. Therefore, this study investigated the function of SpoT in H. pylori resistance to CLA by examining the shifts in the expression of transporters and explored the role of transporters in the CLA resistance of H. pylori. A ΔspoT strain was constructed in this study, and it was shown that SpoT is involved in H. pylori tolerance of CLA by upregulating the transporters HP0939, HP1017, HP0497, and HP0471. This was assessed using a series of molecular and biochemical experiments and a cDNA microarray. Additionally, the knockout of genes hp0939, hp0471, and hp0497 in the resistant strains caused a reduction or loss (the latter in the Δhp0497 strain) of resistance to CLA. Furthermore, the average expression levels of these four transporters in clinical CLA-resistant strains were considerably higher than those in clinical CLA-sensitive strains. Taken together, our results revealed a novel molecular mechanism of H. pylori adaption to CLA stress.

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Section: Methodsmentioning

confidence: 99%

The Bifunctional Enzyme SpoT Is Involved in the Clarithromycin Tolerance of Helicobacter pylori by Upregulating the Transporters HP0939, HP1017, HP0497, and HP0471

Geng

Chen

et al. 2017

Antimicrob Agents Chemother

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Characterisation of point mutations in domain V of the 23S rRNA gene of clinical Helicobacter pylori strains and clarithromycin-resistant phenotype in central Vietnam

Tran

et al. 2019

Journal of Global Antimicrobial Resistance

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Clarithromycin resistance and 23S rRNA gene mutation characteristics of Helicobacter pylori isolates from patients in Qiannan Autonomous Prefecture

Cited by 2 publications

References 0 publications

The Bifunctional Enzyme SpoT Is Involved in the Clarithromycin Tolerance of Helicobacter pylori by Upregulating the Transporters HP0939, HP1017, HP0497, and HP0471

The Bifunctional Enzyme SpoT Is Involved in the Clarithromycin Tolerance of Helicobacter pylori by Upregulating the Transporters HP0939, HP1017, HP0497, and HP0471

Characterisation of point mutations in domain V of the 23S rRNA gene of clinical Helicobacter pylori strains and clarithromycin-resistant phenotype in central Vietnam

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