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首页> 外文期刊>Infection and immunity >Factors responsible for increased susceptibility of mice to intestinal colonization after treatment with streptomycin.
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Factors responsible for increased susceptibility of mice to intestinal colonization after treatment with streptomycin.

机译:链霉素治疗后导致小鼠对肠道菌落敏感性增加的因素。

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摘要

Streptomycin sulfate (5 mg/ml) was added to the drinking water of Swiss white mice. After treatment for 1 week, the mice were challenged orogastrically with 10(8) Pseudomonas aeruginosa cells. The organism failed to multiply in the intestinal tract of either treated or untreated animals, but could be recovered from contents and tissues after 48 h. In a previous study, Salmonella typhimurium was shown to multiply in the intestines of streptomycin-treated but not untreated mice when 10(3) organisms were used as inoculum. Streptomycin administration had little effect on Eh, protein or carbohydrate concentrations of cecal contents, or intestinal motility. However, it caused a statistically significant increase in water content and pH of contents and a decrease in the concentrations of acetic, propionic, butyric, and valeric acids. S. typhimurium multiplied in pooled cecal contents obtained from both streptomycin-treated and untreated animals, but its multiplication rate and total populations were significantly greater in contents from treated animals. P. aeruginosa did not multiply in contents from either treated or untreated mice. Similar results were obtained when the organisms were inoculated into nutrient broth adjusted to simulate the pH levels and volatile fatty acid (VFA) concentrations in cecal contents of treated and untreated mice. The addition of brain heart infusion broth to cecal contents from untreated animals, in concentrations that support multiplication of S. typhimurium and P. aeruginosa, did not reverse inhibition. The addition of VFA to cecal contents from treated animals to equal the concentration in cecal contents from untreated animals caused inhibition of a magnitude observed in cecal contents from untreated animals. The results indicate that VFA operating at the pH level of cecal contents of conventional mice inhibit the multiplication of both S. typhimurium and P. aeruginosa and restrict colonization of the intestine by these organisms. The decrease in VFA concentrations that occurs as a result of streptomycin administration adequately explains the increased susceptibility of treated mice to colonization with S. typhimurium. It does not explain the increased susceptibility of treated mice to P. aeruginosa colonization, however.
机译:将硫酸链霉素(5 mg / ml)添加到瑞士白色小鼠的饮用水中。治疗1周后,用10(8)铜绿假单胞菌细胞经口胃攻击小鼠。该有机体在治疗或未治疗的动物的肠道中均无法繁殖,但可以在48小时后从内含物和组织中恢复出来。在先前的研究中,鼠伤寒沙门氏菌在使用链霉素处理的10(3)种细菌中,在链霉素处理的小鼠的肠道中繁殖,但未经处理的小鼠则没有。链霉素的施用对Eh,盲肠内容物的蛋白质或碳水化合物浓度或肠蠕动几乎没有影响。然而,它引起含水量和内容物的pH在统计学上显着增加,并且乙酸,丙酸,丁酸和戊酸的浓度降低。鼠伤寒沙门氏菌乘以从链霉素治疗和未治疗的动物中收集的盲肠内含物,但其繁殖率和总种群中经处理的动物的内含物明显更大。铜绿假单胞菌在治疗或未治疗小鼠中的含量均未增加。当将生物体接种到经过调整的营养肉汤中以模拟pH值和盲肠内容物中经处理和未经处理的小鼠中的挥发性脂肪酸(VFA)浓度时,可获得相似的结果。在未经处理的动物的盲肠内容物中添加脑心浸液,其浓度可支持鼠伤寒沙门氏菌和铜绿假单胞菌的繁殖,但不能逆转抑制作用。在处理动物的盲肠内容物中添加VFA,使其等于未处理动物的盲肠内容物中的浓度,导致抑制了在未处理动物的盲肠内容物中观察到的大小。结果表明,VFA在常规小鼠的盲肠内含物的pH值水平下运行,可抑制鼠伤寒沙门氏菌和铜绿假单胞菌的繁殖,并限制这些生物在肠道中的定殖。链霉素给药引起的VFA浓度降低充分说明了治疗小鼠对鼠伤寒沙门氏菌定植的敏感性增加。但是,这不能解释经处理的小鼠对铜绿假单胞菌定植的敏感性增加。

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