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首页> 外文期刊>Infection and immunity >Physiological basis of the low calcium response in Yersinia pestis.
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Physiological basis of the low calcium response in Yersinia pestis.

机译：鼠疫耶尔森菌中低钙反应的生理基础。

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It is established that duplication in vitro of that amount of Ca2+ (2.5 mM) and Mg2+ (1.5 mM) present in blood permits vegetative growth of Yersinia pestis with repression of virulence factors encoded by the Lcr plasmid (Lcr+); similar simulation of intracellular fluid (no Ca2+ and 20 mM Mg2+) promotes bacteriostasis with induction of these virulence determinants. However, proliferation of yersiniae in mice occurs primarily within necrotic focal lesions (supplied by Ca(2+)-deficient host cell cytoplasm) within visceral organs rather than in Ca(2+)-sufficient blood. The present study addressed this enigma by defining conditions necessary for achieving vegetative growth of Lcr+ yersiniae at 37 degrees C in simulated intracellular fluid. Maximum optical densities were increased by substitution of K+ for Na+ and elimination of Cl-; the combination of Na+ plus L-glutamate was selectively toxic to Lcr+ cells. This phenomenon was attributed in part to the absence of aspartase in Y. pestis (a lesion known to facilitate massive accumulation of L-aspartate via transamination of the oxalacetate pool by L-glutamate). Replacement of L-glutamate by exogenous L-aspartate or alpha-ketoglutarate reversed this toxicity by favoring retention of oxalacetate. Proliferation of Lcr+ cells in a medium containing K+ and L-aspartate but lacking added Ca2+ and Na+ was markedly enhanced by increasing the concentration of fermentable carbohydrate. Accordingly, in the worst-case scenario (i.e., added Na+, Cl-, and L-glutamate), Lcr+ yersiniae underwent restriction of growth after one doubling, and in the best-case scenario (i.e., added K+ and L-aspartate), the organisms completed more than five doublings, thereby achieving full-scale growth. Both of these Ca(2+)-deficient media promoted maximum induction of Mg(2+)-induced V antigen, a virulence factor encoded by the Lcr plasmid.
机译：已经确定，体外复制血液中存在的一定量的Ca2 +（2.5 mM）和Mg2 +（1.5 mM）可以使鼠疫耶尔森氏菌营养生长，并抑制Lcr质粒（Lcr +）编码的毒力因子。细胞内液（无Ca2 +和20 mM Mg2 +）的类似模拟可通过诱导这些毒力决定因素来促进抑菌作用。但是，耶尔森氏菌在小鼠中的增殖主要发生在内脏器官内的坏死性局灶性病变（由Ca（2+）缺乏宿主细胞的细胞质提供）内，而不是在Ca（2+）充足的血液内。本研究通过定义在37℃下在模拟细胞内液中实现Lcr +耶尔森氏菌营养生长所需的条件，解决了这一难题。通过用K +代替Na +和消除Cl-可以提高最大光密度。 Na +加L-谷氨酸的组合对Lcr +细胞具有选择性毒性。该现象部分归因于鼠疫耶尔森氏菌（已知通过L-谷氨酸对草酰乙酸池进行氨基转移而促进L-天冬氨酸的大量积累的病变）中不存在天冬氨酸酶。用外源性L-天冬氨酸盐或α-酮戊二酸盐代替L-谷氨酸盐可通过保留草酰乙酸来逆转这种毒性。 Lcr +细胞在含有K +和L-天冬氨酸但缺乏添加的Ca2 +和Na +的培养基中的增殖通过增加可发酵碳水化合物的浓度而显着增强。因此，在最坏的情况下（即添加Na +，Cl-和L-谷氨酸），Lcr +耶尔森菌在生长一倍后受到生长的限制，而在最好的情况下（即添加K +和L-天冬氨酸） ，生物体完成了五倍以上的繁殖，从而实现了全面的生长。这两个Ca（2+）缺乏媒体都促进了Mg（2+）诱导的V抗原（由Lcr质粒编码的毒力因子）的最大诱导。

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