Mechanism of growth inhibition by free bile acids in lactobacilli and bifidobacteria
Mechanism of growth inhibition by free bile acids in lactobacilli and bifidobacteria
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DOI：
10.1128/jb.188.5.1979-1986.2006
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发表时间：
2006-03-01
影响因子：
3.2
通讯作者：
Yokota, A
中科院分区：
文献类型：
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作者：
Kurdi, P;Kawanishi, K;Yokota, A
研究了游离胆汁酸（FBAs）、胆酸（CA）、脱氧胆酸（DCA）和鹅脱氧胆酸（chenodeoxycholic acid）对乳酸杆菌和双歧杆菌生物能量学和生长的影响。结果发现，这些FBAs降低了这些细菌的内部pH值与快速和逐步的动力学，并在一定浓度下，消散Δ pH值。消散Δ pH值的胆汁酸浓度对应于选定的细菌的MIC。与乙酸盐、丙酸盐和丁酸盐不同，FBAs耗散跨膜电位（Δ psi）。在短双歧杆菌JCM 1192中，合成的质子导体五氯苯酚（PCP）在比FBA低得多的浓度下以缓慢和连续的动力学消散Delta pH，这表明FBA和真正的质子导体之间的作用模式不同。通过荧光法评估的膜损伤和活力下降也观察到接触CA或DCA在MIC，但没有五氯苯酚或短链脂肪酸混合物。在CA浓度大于2 mM（0.4x MIC）时观察到钾离子损失，而在CA浓度大于4 mM（0.8x MIC）时其他细胞组分的泄漏增加。此外，在实验中，膜磷脂囊泡提取唾液乳杆菌亚种。水杨酸JCM 1044、CA和DCA在MIC下使ApH崩溃，伴随囊内荧光pH探针的泄漏，而它们在较低浓度范围下没有显示质子电导（例如，0.2x MIC）。将这些观察结果结合在一起，我们得出结论，在MIC下的FBAs干扰膜完整性，并且这种效应可导致质子（膜ApH和A-If耗散）、钾离子和其他细胞组分的泄漏，并最终导致细胞死亡。
The effects of the free bile acids (FBAs) cholic acid (CA), deoxycholic acid (DCA), and chenodeoxycholic acid on the bioenergetics and growth of lactobacilli and bifidobacteria were investigated. It was found that these FBAs reduced the internal pH levels of these bacteria with rapid and stepwise kinetics and, at certain concentrations, dissipated Delta pH. The bile acid concentrations that dissipated Delta pH corresponded with the MICs for the selected bacteria. Unlike acetate, propionate, and butyrate, FBAs dissipated the transmembrane electrical potential (Delta psi). In Bifidobacterium breve JCM 1192, the synthetic proton conductor pentachlorophenol (PCP) dissipated Delta pH with a slow and continuous kinetics at a much lower concentration than FBAs did, suggesting the difference in mode of action between FBAs and true proton conductors. Membrane damage assessed by the fluorescence method and a viability decrease were also observed upon exposure to CA or DCA at the MIC but not to PCP or a short-chain fatty acid mixture. Loss of potassium ion was observed at CA concentrations more than 2 mM (0.4x MIC), while leakage of other cellular components increased at CA concentrations more than 4 mM (0.8x MIC). Additionally, in experiments with membrane phospholipid vesicles extracted from Lactobacillus salivarius subsp. salicinius JCM 1044, CA and DCA at the MIC collapsed the ApH with concomitant leakage of intravesicular fluorescent pH probe, while they did not show proton conductance at a lower concentration range (e.g., 0.2x MIC). Taking these observations together, we conclude that FBAs at the MIC disturb membrane integrity and that this effect can lead to leakage of proton (membrane ApH and A-If dissipation), potassium ion, and other cellular components and eventually cell death.