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鼠疫耶尔森菌对杀鼠菌素的抗性、铁储存及对HeLa细胞的侵袭

Resistance to pesticin, storage of iron, and invasion of HeLa cells by Yersiniae.

作者信息

Sikkema D J, Brubaker R R

出版信息

Infect Immun. 1987 Mar;55(3):572-8. doi: 10.1128/iai.55.3.572-578.1987.

DOI:10.1128/iai.55.3.572-578.1987
PMID:3818085
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC260376/
Abstract

The independent abilities of Yersinia pestis to absorb exogenous pigments including hemin and Congo red (Pgm+) and to produce the bacteriocin pesticin with genetically linked invasive enzymes (Pst+) are established virulence factors of the species. Pst- Pgm+ strains of Y. pestis are sensitive to pesticin (Psts), and mutation of these isolates to pesticin resistance (Pstr) is known to result in concomitant conversion to Pgm-. Wild-type cells of Yersinia pseudotuberculosis and Yersinia enterocolitica are Pgm- but may be Psts; mutation of the latter to Pstr also results in avirulence. In this study, typical Pgm- mutants of Y. pestis exhibited a dramatic nutritional requirement at 37 degrees C but not 26 degrees C for iron which could be fulfilled by either Fe3+ or hemin. Iron privation of Pgm- yersiniae resulted in formation of osmotically stable spheroplasts similar to those previously observed after exposure of Psts bacteria to pesticin. At 37 degrees C, Pgm+ organisms rapidly overgrew initially predominant Pgm- populations in iron-deficient medium. However, Pgm-isolates could undergo a second mutation that permitted successful competition with Pgm+ cells in this environment. The mutation to Pstr in Y. pseudotuberculosis and Y. enterocolitica did not promote a similar requirement for iron but rather prevented these organisms from penetrating HeLa cells. The ability to invade these nonprofessional phagocytes was not shared by Pgm+ or Pgm- cells of Y. pestis.

摘要

鼠疫耶尔森菌吸收包括血红素和刚果红(Pgm+)在内的外源性色素以及产生与具有遗传连锁侵袭酶的细菌素鼠疫菌素(Pst+)的独立能力是该物种已确定的毒力因子。鼠疫耶尔森菌的Pst - Pgm+菌株对鼠疫菌素(Psts)敏感,已知这些分离株突变为对鼠疫菌素耐药(Pstr)会导致同时转变为Pgm-。假结核耶尔森菌和小肠结肠炎耶尔森菌的野生型细胞是Pgm-,但可能是Psts;后者突变为Pstr也会导致无毒力。在本研究中,鼠疫耶尔森菌典型的Pgm-突变体在37℃时对铁有显著的营养需求,而在26℃时则没有,铁可以由Fe3+或血红素满足。Pgm-耶尔森菌缺铁会导致形成渗透压稳定的原生质球,类似于之前在Psts细菌接触鼠疫菌素后观察到的情况。在37℃时,Pgm+生物体在缺铁培养基中迅速超过最初占优势的Pgm-群体。然而,Pgm-分离株可能会发生第二次突变,从而在这种环境中与Pgm+细胞成功竞争。假结核耶尔森菌和小肠结肠炎耶尔森菌突变为Pstr并没有促进对铁的类似需求,而是阻止了这些生物体穿透HeLa细胞。鼠疫耶尔森菌的Pgm+或Pgm-细胞不具备侵入这些非专职吞噬细胞的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e8/260376/00f5a10beb90/iai00087-0087-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e8/260376/00f5a10beb90/iai00087-0087-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9e8/260376/00f5a10beb90/iai00087-0087-a.jpg

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Iron (II) inactivation of myeloperoxidase.铁(II)使髓过氧化物酶失活。
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A study on pesticin biosynthesis.关于杀有害物菌素生物合成的研究。
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Genome-wide mutant fitness profiling identifies nutritional requirements for optimal growth of Yersinia pestis in deep tissue.全基因组突变体适应性分析确定了鼠疫耶尔森菌在深部组织中最佳生长的营养需求。
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Functional and structural analysis of HicA3-HicB3, a novel toxin-antitoxin system of Yersinia pestis.鼠疫耶尔森氏菌新型毒素-抗毒素系统HicA3-HicB3的功能与结构分析
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HeLa cell infection by Yersinia enterocolitica: evidence for lack of intracellular multiplication and development of a new procedure for quantitative expression of infectivity.小肠结肠炎耶尔森菌对海拉细胞的感染:缺乏细胞内增殖的证据及一种新的感染性定量表达方法的建立
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