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首页> 外文期刊>Applied and Environmental Microbiology >Bioenergetic Mechanism for Nisin Resistance, Induced by the Acid Tolerance Response of Listeria monocytogenes
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Bioenergetic Mechanism for Nisin Resistance, Induced by the Acid Tolerance Response of Listeria monocytogenes

机译：单核细胞增生性李斯特菌的耐酸性诱导的乳链菌肽抗性的生物能机制

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This study examined the bioenergetics of Listeria monocytogenes, induced to an acid tolerance response (ATR). Changes in bioenergetic parameters were consistent with the increased resistance of ATR-induced (ATR+) cells to the antimicrobial peptide nisin. These changes may also explain the increased resistance of L. monocytogenes to other lethal factors. ATR+ cells had lower transmembrane pH (ΔpH) and electric potential (Δψ) than the control (ATR?) cells. The decreased proton motive force (PMF) of ATR+ cells increased their resistance to nisin, the action of which is enhanced by energized membranes. Paradoxically, the intracellular ATP levels of the PMF-depleted ATR+ cells were ～7-fold higher than those in ATR? cells. This suggested a role for the FoF1 ATPase enzyme complex, which converts the energy of ATP hydrolysis to PMF. Inhibition of the FoF1 ATPase enzyme complex by N′-N′-1,3-dicyclohexylcarbodiimide increased ATP levels in ATR? but not in ATR+ cells, where ATPase activity was already low. Spectrometric analyses (surface-enhanced laser desorption ionization-time of flight mass spectrometry) suggested that in ATR+ listeriae, the downregulation of the proton-translocating c subunit of the FoF1 ATPase was responsible for the decreased ATPase activity, thereby sparing vital ATP. These data suggest that regulation of FoF1 ATPase plays an important role in the acid tolerance response of L. monocytogenes and in its induced resistance to nisin.
机译：这项研究检查了单核细胞增多性李斯特菌的生物能，诱导了其对酸的耐受性反应（ATR）。生物能参数的变化与ATR诱导的（ATR +）细胞对抗菌肽乳链菌肽的抗性增加相一致。这些变化也可以解释单核细胞增生李斯特氏菌对其他致死因子的耐药性增加。 ATR +细胞的跨膜pH（ΔpH）和电势（Δψ）低于对照（ATR3）细胞。 ATR +细胞的质子动力（PMF）降低，增加了其对乳链菌肽的抵抗力，这种作用被通电的膜增强。矛盾的是，PMF耗尽的ATR +细胞的细胞内ATP水平比ATR？细胞高约7倍。细胞。这暗示了FoF1 ATPase酶复合物的作用，该复合物将ATP水解的能量转换为PMF。 N'-N'-1,3-二环己基碳二亚胺对FoF1 ATP酶复合物的抑制作用会增加ATR中的ATP水平。但是在ATPase活性已经很低的ATR +细胞中却没有。光谱分析（表面增强的激光解吸电离飞行时间质谱）表明，在ATR +李斯特菌中，FoF1 ATPase质子移位c亚基的下调导致ATPase活性降低，从而节省了重要的ATP。这些数据表明，FoF1 ATPase的调控在单核细胞增生李斯特氏菌的酸耐受反应及其对乳链菌肽的抗性中起重要作用。

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