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Insertion of mini-IS605 and deletion of adjacent sequences in the nitroreductase (rdxA) gene cause metronidazole resistance in Helicobacter pylori NCTC11637.微小插入序列IS605插入及相邻序列缺失导致幽门螺杆菌NCTC11637的硝基还原酶（rdxA）基因产生甲硝唑耐药性。
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2
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本文引用的文献

1
Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori.人类胃部病原体幽门螺杆菌两个不相关分离株的基因组序列比较。
Nature. 1999 Jan 14;397(6715):176-80. doi: 10.1038/16495.
2
Novel sequence organization and insertion specificity of IS605 and IS606: chimaeric transposable elements of Helicobacter pylori.IS605和IS606的新型序列组织与插入特异性：幽门螺杆菌的嵌合转座元件
Gene. 1998 Nov 26;223(1-2):175-86. doi: 10.1016/s0378-1119(98)00164-4.
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Epidemiology and mechanism of antibiotic resistance in Helicobacter pylori.幽门螺杆菌抗生素耐药性的流行病学及机制
Gastroenterology. 1998 Nov;115(5):1278-82. doi: 10.1016/s0016-5085(98)70101-5.
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Antibiotic resistance in Helicobacter pylori: implications for therapy.幽门螺杆菌的抗生素耐药性：对治疗的影响。
Gastroenterology. 1998 Nov;115(5):1272-7. doi: 10.1016/s0016-5085(98)70100-3.
5
Explaining the bias in the 23S rRNA gene mutations associated with clarithromycin resistance in clinical isolates of Helicobacter pylori.解释幽门螺杆菌临床分离株中与克拉霉素耐药相关的23S rRNA基因突变的偏差。
Antimicrob Agents Chemother. 1998 Oct;42(10):2749-51. doi: 10.1128/AAC.42.10.2749.
6
Metronidazole resistance in Helicobacter pylori is due to null mutations in a gene (rdxA) that encodes an oxygen-insensitive NADPH nitroreductase.幽门螺杆菌对甲硝唑耐药是由于一个编码对氧不敏感的NADPH硝基还原酶的基因（rdxA）发生无效突变所致。
Mol Microbiol. 1998 Apr;28(2):383-93. doi: 10.1046/j.1365-2958.1998.00806.x.
7
Analyses of the cag pathogenicity island of Helicobacter pylori.幽门螺杆菌cag致病岛的分析
Mol Microbiol. 1998 Apr;28(1):37-53. doi: 10.1046/j.1365-2958.1998.00770.x.
8
Simple and efficient generation in vitro of nested deletions and inversions: Tn5 intramolecular transposition.体外简单高效地产生嵌套缺失和倒位：Tn5分子内转座。
Nucleic Acids Res. 1998 Apr 15;26(8):1927-33. doi: 10.1093/nar/26.8.1927.
9
Corrected identity of isolates of Helicobacter pylori reference strain NCTC11637.幽门螺杆菌参考菌株NCTC11637分离株的校正身份
Helicobacter. 1997 Mar;2(1):48-52. doi: 10.1111/j.1523-5378.1997.tb00058.x.
10
Metronidazole resistance reduces efficacy of triple therapy and leads to secondary clarithromycin resistance.甲硝唑耐药会降低三联疗法的疗效，并导致继发性克拉霉素耐药。
Dig Dis Sci. 1997 Oct;42(10):2111-5. doi: 10.1023/a:1018882804607.

微小插入序列IS605插入及相邻序列缺失导致幽门螺杆菌NCTC11637的硝基还原酶（rdxA）基因产生甲硝唑耐药性。

Insertion of mini-IS605 and deletion of adjacent sequences in the nitroreductase (rdxA) gene cause metronidazole resistance in Helicobacter pylori NCTC11637.

作者信息

Debets-Ossenkopp Y J, Pot R G, van Westerloo D J, Goodwin A, Vandenbroucke-Grauls C M, Berg D E, Hoffman P S, Kusters J G

机构信息

Department of Medical Microbiology, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands.

出版信息

Antimicrob Agents Chemother. 1999 Nov;43(11):2657-62. doi: 10.1128/AAC.43.11.2657.

DOI:10.1128/AAC.43.11.2657
PMID:10543743
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC89539/
Abstract

We found that NCTC11637, the type strain of Helicobacter pylori, the causative agent of peptic ulcer disease and an early risk factor for gastric cancer, is metronidazole resistant. DNA transformation, PCR-based restriction analysis, and DNA sequencing collectively showed that the metronidazole resistance of this strain was due to mutation in rdxA (gene HP0954 in the full genome sequence of H. pylori 26695) and that resistance did not depend on mutation in any of the other genes that had previously been suggested: catalase (katA), ferredoxin (fdx), flavodoxin (fldA), pyruvate:flavodoxin oxidoreductase (porgammadeltaalphabeta), RecA (recA), or superoxide dismutase (sodB). This is in accord with another recent study that attributed metronidazole resistance to point mutations in rdxA. However, the mechanism of rdxA inactivation that we found in NCTC11637 is itself also novel: insertion of mini-IS605, one of the endogenous transposable elements of H. pylori, and deletion of adjacent DNA sequences including 462 bp of the 851-bp-long rdxA gene.

摘要

我们发现，幽门螺杆菌的模式菌株NCTC11637对甲硝唑耐药，幽门螺杆菌是消化性溃疡疾病的病原体及胃癌的早期危险因素。DNA转化、基于PCR的限制性分析和DNA测序共同表明，该菌株对甲硝唑耐药是由于rdxA（幽门螺杆菌26695全基因组序列中的HP0954基因）发生突变，且耐药性不依赖于之前提出的任何其他基因的突变：过氧化氢酶（katA）、铁氧化还原蛋白（fdx）、黄素氧化还原蛋白（fldA）、丙酮酸：黄素氧化还原蛋白氧化还原酶（porgammadeltaalphabeta）、RecA（recA）或超氧化物歧化酶（sodB）。这与最近另一项将甲硝唑耐药归因于rdxA点突变的研究一致。然而，我们在NCTC11637中发现的rdxA失活机制本身也是新颖的：mini-IS605（幽门螺杆菌的内源性转座元件之一）插入，以及包括851 bp长的rdxA基因中462 bp的相邻DNA序列缺失。