Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quinolone antibiotics at sub-inhibitory concentrations have been shown to antagonize the adherence of Escherichia coli to urinary tract epithelium. This may be due either to reduced expression or to alterations to the structure of the fimbriae which mediate adherence. While E. coli cells 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 PD131628 at a concentration equivalent to 0.5 x MIC. An in-vitro adherence assay which used acid-washed uroepithelial cells and a type 1-fimbriated strain of E. coli showed 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, fimB and fimE, and the main structural gene, fimA, were evaluated by quantifying beta-galactosidase production encoded by chromosomally-located fim::lacZ fusions. All four quinolones tested caused reductions in beta-galactosidase production by a fimA::lacZ fusion strain, but did not significantly affect production of this enzyme by fimB::lacZ and fimE::lacZ fusion strains; these agents also led to decreases in wild-type beta-galactosidase production. Amplification of the invertible element after exposure to enoxacin at 0.25, 0.5 or 1 x 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 x MIC.
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PMID:Modulation of Escherichia coli type 1 fimbrial expression and adherence to uroepithelial cells following exposure of logarithmic phase cells to quinolones at subinhibitory concentrations. 781 81

The mechanisms by which quinolones rapidly kill are ill defined. We have investigated the action of ciprofloxacin on Escherichia coli KL16 with a combination of traditional and flow cytometric methods and have analyzed cells for changes in membrane potential, membrane integrity, oxidative metabolism, morphology, and viability. Log-phase cultures were exposed to various concentrations (0.1, 1, 10, and 100 times the MIC) of ciprofloxacin and analyzed at regular intervals over 120 min. We also measured protein synthesis in the related strain PQ37 cultured under the same conditions over 300 min, using a colorimetric assay for beta-galactosidase release. Despite a 3-log order decrease in CFU after 60-min exposure to 10 and 100 times the MIC of ciprofloxacin, there was no equivalent decrease in bacterial numbers as determined by both light microscopy and flow cytometry. Furthermore, while these bacteria showed concentration-dependent morphological changes, most were capable not only of excluding the fluorescent nucleic acid-binding dye propidium iodide, but also of reducing the tetrazolium dye cyanoditodyl tetrazolium chloride. Over 90% of the bacteria maintained a membrane potential [as determined by exclusion of bis-[1,3-dibutylbarbituric acid) trimethine oxonol] when exposed to ciprofloxacin for 120 min, except at 100 times the MIC, when this figure fell to < 10%. Finally, protein synthesis was either maintained or induced at all concentrations of ciprofloxacin up to 5 h postexposure. Taken together, these results demonstrate the continuing physical and metabolic survival of ciprofloxacin-exposed bacteria; we suggest parallels with the concept of the viable nonculturable state.
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PMID:Antibacterial action of ciprofloxacin. 859 14

Resistance to piperacillin in several isolates of Citrobacter freundii and Enterobacter cloacae was investigated and confirmed to occur at a frequency of 10(-7) to 10(-6). Development of resistance to piperacillin was significantly suppressed by tazobactam but not by clavulanic acid. To elucidate the mechanism by which resistance suppression occurs, the effect of piperacillin plus tazobactam on the induction of AmpC beta-lactamase was analyzed by monitoring the beta-galactosidase activity of an inducible ampC-lacZ gene fusion in Escherichia coli. The combination exerted no inhibitory effect on AmpC beta-lactamase induction. Tazobactam also had no effect on the accumulation of a key intermediate in the AmpC beta-lactamase induction pathway, 1,6-anhydromurotripeptide, in an ampD mutant strain of E. coli. However, the addition of tazobactam to liquid cultures of E. cloacae 40001 in the presence of piperacillin at four times the MIC caused a delay in the recovery of the culture to piperacillin-induced stress. At 16 times the MIC, a complete suppression of regrowth occurred. Analysis of culture viability on piperacillin plates showed that the culture recovery was due to growth by moderately resistant mutants preexisting in the cell population, which at 16 times the MIC became susceptible to the combination. Evidence from the kinetics of inhibition of the E. cloacae 40001 AmpC beta-lactamase by clavulanic acid, sulbactam, and tazobactam and from the effects of these drugs on the frequency of resistance to piperacillin suggests that the suppressive effect of tazobactam on the appearance of resistance is primarily mediated by the beta-lactamase inhibitory activity.
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PMID:Mechanism of suppression of piperacillin resistance in enterobacteria by tazobactam. 933 44

The first step in ergosterol biosynthesis in Saccharomyces cerevisiae consists of the condensation of two acetyl coenzyme A (acetyl-CoA) moieties by acetoacetyl-CoA thiolase, encoded by ERG10. The inhibition of the sterol pathway results in feedback activation of ERG10 transcription. A cell-based reporter assay, in which increased ERG10 transcription results in elevated specific beta-galactosidase activity, was used to find novel inhibitors of ergosterol biosynthesis that could serve as chemical starting points for the development of novel antifungal agents. A class of pyridines and pyrimidines identified in this way had no detectable activity against the major fungal pathogen Candida albicans (MICs > 64 micro g. ml(-1)). However, a strain of C. albicans lacking the Cdr1p and Cdr2p efflux pumps was sensitive to the compounds (with MICs ranging from 2 to 64 micro g. ml(-1)), suggesting that they are efficiently removed from wild-type cells. Quantitative analysis of sterol intermediates that accumulated during growth inhibition revealed the accumulation of lanosterol at the expense of ergosterol. Furthermore, a clear correlation was found between the 50% inhibitory concentration at which the sterol profile was altered and the antifungal activity, measured as the MIC. This finding strongly suggests that the inhibition of growth was caused by a reduction in ergosterol synthesis. The compounds described here are a novel class of antifungal pyridines and pyrimidines and the first pyri(mi)dines to be shown to putatively mediate their antifungal activity against C. albicans via lanosterol demethylase.
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PMID:Pyridines and pyrimidines mediating activity against an efflux-negative strain of Candida albicans through putative inhibition of lanosterol demethylase. 1469 56

This study was conducted to determine the effect of antibiotic stress on the virulence factor expression, simulated gastric fluid (SGF; pH 1.5) survival, and heat tolerance (56 degrees C) of Escherichia coli O157:H7. The MIC for three antibiotics (trimethoprim, ampicillin, and ofloxacin) was determined for two E. coli O157:H7 strains (ATCC 43895 [raw hamburger isolate] and ATCC 43890 [fecal isolate]) by the dilution series method. Subsequently, cells were stressed at the MIC of each antibiotic for 4 h, and poststress tolerance and virulence factor production were evaluated. Heat tolerance (56 degrees C) was determined by the capillary tube method, and SGF (pH 1.5) survival was used to assess acid tolerance. Virulence factor expression (stx, hlyA, and eaeA) was evaluated by the creation of lacZ gene fusions and then use of the Miller assay (a beta-galactosidase assay). Stressed and control cells were evaluated in triplicate. The MIC for trimethoprim was 0.26 mg/liter for both strains; for ampicillin, it was 2.05 mg/liter for both strains; and for ofloxacin, it was 0.0256 and 0.045 mg/liter for each strain. Heat tolerance and SGF survival following antibiotic stress decreased when compared with control cells (P < 0.05). Exposure to ofloxacin increased stx and eaeA expression (P < 0.05). Exposure to ampicillin or trimethoprim increased eaeA expression (P < 0.05). hly expression increased following trimethoprim stress (P < 0.05). Antibiotics can increase E. coli O157:H7 virulence factor production, but they do not produce a cross-protective response to heat or decreased pH.
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PMID:Impact of antibiotic stress on acid and heat tolerance and virulence factor expression of Escherichia coli O157:H7. 1726 80

As Gardnerella vaginalis is accepted as a member of normal vaginal flora, it is one of the dominant species which has been related to bacterial vaginosis (BV). The aim of this study was to determine the isolation rate, biotypes and antibiotic resistance patterns of G.vaginalis from the vaginal swab samples of 408 women who were admitted to the outpatient clinics of Family Planning Center. Hippurate hydrolysis, lipase and beta-galactosidase tests were performed for biotyping the isolates, and agar dilution (for metronidazole) and disk diffusion (for clindamycin) tests were used for the detection of antibiotic resistance patterns. As a result, by Nugent's BV scoring protocol, 122 (29.9%), 20 (29.4%), 137 (33.6%), and 18 (4.4%) of the women were diagnosed as BV, intermediate form, normal vaginal flora (NVF) and mycotic vaginosis, respectively. The overall isolation rate of G.vaginalis was found as 23% (94/408). Of them, 56.4% (53/94) and 8.5% (8/94) were isolated from samples of BV cases and subjects with NVF, respectively, and the difference was statistically significant (p<0.05). The biotyping results showed that the most frequently detected types were biotype 1 (44%), 5 (20%) and 4 (18%). There was no statistically significant difference between the biotype distribution of BV patients and the subjects who have NVF (p=0.687). The results of antibiotic susceptibility tests indicated that 70% and 53% of the isolates were resistant to metronidazole and clindamycin, respectively. It was of interest that MIC values for metronidazole was > or =128 microg/ml in 57% of resistant strains. The data of this study has emphasized that the metronidazole resistance is very high in our population, and the large scale studies are needed to clarify the relationship between BV and G.vaginalis biotypes, which can be found in the normal vaginal flora.
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PMID:[Biotypes and antibiotic resistance patterns of Gardnerella vaginalis strains isolated from healthy women and women with bacterial vaginosis]. 1742 49