Factors responsible for increased susceptibility of mice to intestinal colonization after treatment with streptomycin

Factors responsible for increased susceptibility of mice to intestinal colonization after treatment with streptomycin
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链霉素治疗后小鼠肠道定植易感性增加的因素

DOI:
10.1128/iai.53.1.116-123.1986
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发表时间:
1986
影响因子:
3.1
通讯作者:
D. Hentges
D. Hentges
中科院分区:
医学2区
文献类型:
--
作者:
J. Que;S. Casey;D. Hentges

文献摘要

被引文献

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将硫酸链霉素(5 mg/ml)加入到瑞士小白鼠的饮用水中。治疗1周后,小鼠腹腔注射10(8)个铜绿假单胞菌细胞。在先前的一项研究中,当10(3)种沙门氏菌作为接种物时,鼠伤寒沙门菌在链霉素处理的小鼠肠道中繁殖,而在未处理的小鼠肠道中繁殖。链霉素给药对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,它引起了含量和pH值的统计学显著增加,乙酸、丙酸、丁酸和戊酸浓度的降低。鼠伤寒沙门氏菌在链霉素处理和未处理动物的盲肠内容物中增殖,但在处理动物的内容物中增殖率和种群总数显著高于处理动物。铜绿假单胞菌在处理或未处理小鼠的内容物中均未繁殖。将这些微生物接种到模拟处理和未处理小鼠盲肠内容物pH值和挥发性脂肪酸(VFA)浓度的营养液中,得到了类似的结果。在未处理动物的盲肠内容物中加入脑心灌注汤,其浓度支持鼠伤寒沙门氏菌和铜绿假单胞菌的繁殖,并没有逆转抑制作用。将VFA添加到治疗动物的盲肠内容物中,使其与未治疗动物的盲肠内容物中的浓度相等,对未治疗动物的盲肠内容物产生一定程度的抑制作用。结果表明,在常规小鼠盲肠内容物的pH水平下,VFA可以抑制鼠伤寒沙门氏菌和铜绿假单胞菌的繁殖,并限制这两种微生物在肠道的定植。由于给药链霉素导致VFA浓度下降,这充分解释了治疗小鼠对鼠伤寒沙门氏菌定植的易感性增加。然而,这并不能解释治疗小鼠对铜绿假单胞菌定植的易感性增加。
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.