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首页> 外文期刊>Applied and Environmental Microbiology >Mechanisms of acid resistance in enterohemorrhagic Escherichia coli.
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Mechanisms of acid resistance in enterohemorrhagic Escherichia coli.

机译:肠出血性大肠杆菌中的抗酸机制。

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Enterohemorrhagic strains of Escherichia coli must pass through the acidic gastric barrier to cause gastrointestinal disease. Taking into account the apparent low infectious dose of enterohemorrhagic E. coli, 11 O157:H7 strains and 4 commensal strains of E. coli were tested for their abilities to survive extreme acid exposures (pH 3). Three previously characterized acid resistance systems were tested. These included an acid-induced oxidative system, an acid-induced arginine-dependent system, and a glutamate-dependent system. When challenged at pH 2.0, the arginine-dependent system provided more protection in the EHEC strains than in commensal strains. However, the glutamate-dependent system provided better protection than the arginine system and appeared equally effective in all strains. Because E. coli must also endure acid stress imposed by the presence of weak acids in intestinal contents at a pH less acidic than that of the stomach, the ability of specific acid resistance systems to protect against weak acids was examined. The arginine- and glutamate-dependent systems were both effective in protecting E. coli against the bactericidal effects of a variety of weak acids. The acids tested include benzoic acid (20 mM; pH 4.0) and a volatile fatty acid cocktail composed of acetic, propionic, and butyric acids at levels approximating those present in the intestine. The oxidative system was much less effective. Several genetic aspects of E. coli acid resistance were also characterized. The alternate sigma factor RpoS was shown to be required for oxidative acid resistance but was only partially involved with the arginine- and glutamate-dependent acid resistance systems. The arginine decarboxylase system (including adi and its regulators cysB and adiY) was responsible for arginine-dependent acid resistance. The results suggest that several acid resistance systems potentially contribute to the survival of pathogenic E. coli in the different acid stress environments of the stomach (pH 1 to 3) and the intestine (pH 4.5 to 7 with high concentrations of volatile fatty acids). Of particular importance to the food industry was the finding that once induced, the acid resistance systems will remain active for prolonged periods of cold storage at 4 degrees C.
机译:大肠杆菌的肠出血性菌株必须通过酸性胃屏障以引起胃肠道疾病。考虑到肠出血性大肠杆菌的明显低感染剂量,测试了11株O157:H7菌株和4株大肠杆菌菌株在极端酸暴露(pH 3)下的存活能力。测试了三个先前表征的耐酸系统。这些包括酸诱导的氧化系统,酸诱导的精氨酸依赖性系统和谷氨酸依赖性系统。当在pH 2.0下受到挑战时,精氨酸依赖性系统在EHEC菌株中比在普通菌株中提供了更多的保护。然而,谷氨酸依赖性系统比精氨酸系统提供更好的保护,并且在所有菌株中均表现出相同的效果。因为大肠杆菌还必须在比胃酸弱的pH值下承受肠内物质中存在弱酸而施加的酸胁迫,所以研究了特定的抗酸系统抵抗弱酸的能力。精氨酸和谷氨酸依赖性系统均能有效保护大肠杆菌免受各种弱酸的杀菌作用。测试的酸包括苯甲酸(20 mM; pH 4.0)和由乙酸,丙酸和丁酸组成的挥发性脂肪酸混合物,其含量近似于肠道中的含量。氧化系统的效果要差得多。大肠杆菌酸抗性的几个遗传方面也进行了表征。已显示备用sigma因子RpoS是抗氧化性所必需的,但仅部分依赖于精氨酸和谷氨酸依赖性的抗酸系统。精氨酸脱羧酶系统(包括adi及其调节剂cysB和adiY)负责精氨酸依赖性酸的抵抗。结果表明,几种抗酸系统可能会在胃(pH值为1至3)和肠(pH值为4.5至7,含有高浓度的挥发性脂肪酸)的不同酸胁迫环境中,促进致病性大肠杆菌的存活。对于食品工业而言,特别重要的发现是,一旦被诱导,耐酸系统将在4摄氏度的长时间冷藏中保持活跃。

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