MODULATION OF ESCHERICHIA-COLI TYPE-1 FIMBRIAL EXPRESSION AND ADHERENCE TO UROEPITHELIAL CELLS FOLLOWING EXPOSURE OF LOGARITHMIC PHASE CELLS TO QUINOLONES AT SUBINHIBITORY CONCENTRATIONS
MODULATION OF ESCHERICHIA-COLI TYPE-1 FIMBRIAL EXPRESSION AND ADHERENCE TO UROEPITHELIAL CELLS FOLLOWING EXPOSURE OF LOGARITHMIC PHASE CELLS TO QUINOLONES AT SUBINHIBITORY CONCENTRATIONS
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DOI：
10.1093/jac/34.2.205
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发表时间：
1994-08-01
影响因子：
5.2
通讯作者：
BURNHAM, JC
中科院分区：
文献类型：
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作者：
BREINES, DM;BURNHAM, JC
研究表明，亚抑制浓度的喹诺酮类抗生素可拮抗大肠埃希菌尿路上皮细胞的黏附。这可能是由于表达减少或调节粘连的菌毛结构改变所致。在此期间。处于生长平稳阶段的结肠癌细胞以前曾被用来研究喹诺酮类药物对黏附的抑制作用，本研究证明，处于对数生长期的细菌也会产生1型菌毛，这些微生物的黏附在暴露于各种喹诺酮类药物后会减少。在所有实验中，将处于对数生长期的细胞与浓度相当于0.5×MIC的环丙沙星、依诺沙星、CI-960或PDI31628孵育3h。用酸洗的尿路上皮细胞和一株1型菌毛的E。依诺沙星、环丙沙星和PD131628分别使依诺沙星、环丙沙星和PD131628的粘附率降低47%、72%和95%。通过定量检测染色体定位的fim：：lacZ融合基因编码的β半乳糖苷酶产物，评价了环丙沙星、依诺沙星、CI-96 0和PD1316 2 8对两相变异控制基因fimBandfimE和主要结构基因fimA的影响。所有被测试的四种喹诺酮类药物都能使AFIMA：：lacZfusion菌株的β-半乳糖苷酶产量下降，但对FimB：：lacZandfimE：：lacZfusion菌株的β-半乳糖苷酶产量没有显著影响；这些药物也导致野生型FIMA-半乳糖苷酶产量的下降。依诺沙星作用于0·25、0·5或1×MIC的可逆元件后，与未加抗生素的对照相比，定向分布无明显变化。此外，针对1型菌毛的荧光分析显示，环丙沙星、依诺沙星、CI-960和PD131628分别与环丙沙星、依诺沙星、CI-960和PD131628孵育后，在0.5×MIC时，结构亚单位的表面表达分别下降了23%、21%、25%和11%。
Quinolone antibiotics at sub-inhibitory concentrations have been shown to antagonize the adherence ofEscherichia colito urinary tract epithelium. This may be due either to reduced expression or to alterations to the structure of the fimbriae which mediate adherence. WhileE. colicells in the stationary growth phase have previously been used to investigate quinolone-induced inhibition of adherence, the present study has demonstrated that bacteria in the logarithmic phase also produce type 1 fimbriae and that the adherence of these organisms is reduced following exposure to various quinolones. In all experiments, cells in the logarithmic phase were incubated for 3 h in the presence of ciprofloxacin, enoxacin, CI-960 or PDI31628 at a concentration equivalent to 0.5×MIC. An in-vitro adherence assay which used acid-washed uroepithelial cells and a type 1-fimbriated strain ofE. colishowed reductions in adherence of 47%, 72% and 95% after exposure to enoxacin, ciprofloxacin and PD131628, respectively. The effects of ciprofloxacin, enoxacin, CI-960 and PD131628 on two phase variation controlling genes,fimBandfimE, and the main structural gene,fimA, were evaluated by quantifyingβ-galactosidase production encoded by chromosomally-locatedfim :: lacZfusions. All four quinolones tested caused reductions inβ-galactosidase production by afimA :: lacZfusion strain, but did not significantly affect production of this enzyme byfimB :: lacZandfimE :: lacZfusion strains; these agents also led to decreases in wild-typeβ-galactosidase production. Amplification of the invertible element after exposure to enoxacin at 0·25, 0·5 or 1 × MIC revealed no changes in orientation distribution compared with the antibiotic-free control. In addition, a fluorescence assay specific for type 1 fimbriae showed only 23%, 21%, 25% and 11% reductions in the surface expression of the structural subunit after incubation in the presence of ciprofloxacin, enoxacin, CI-960 and PD131628, respectively, at 0·5 × MIC.