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At least 469 records · Page 26Linked to original sources
PubMed1988

Interactions between antibacterial agents of the quinolone group and nitrofurantoin.

Plate diffusion tests showed that nitrofurantoin antagonized the activity of nalidixic acid, norfloxacin, ciprofloxacin and enoxacin against many Gram-negative bacilli, including all Proteus mirabilis and Klebsiella aerogenes strains tested. No interaction was exhibited when nitrofurantoin and the newer quinolones were tested against Pseudomonas aeruginosa, staphylococci or streptococci. Antagonism was not reliably demonstrated in chessboard titrations, especially with the newer quinolones. Continuous turbidimetric monitoring revealed that antagonism in Pr. mirabilis was associated with abolition of the bacteriolytic response to quinolones and parallel viable counts established that the bactericidal effect of quinolones was suppressed. Apparent potentiation of the effect of nitrofurantoin by nalidixic acid and other quinolones against Pr. mirabilis appeared to be caused by inhibition of swarming into the nitrofurantoin inhibition zone.

Anti-Bacterial Agents↗
PubMed1988

Quantitative study of the interaction between two antibiotics by agar diffusion.

In order to quantify the interaction between two antibiotics by agar diffusion, a fractional critical concentration (FCC) index, analogous to the fractional inhibitory concentration (FIC) index, was defined. Two pairs of filter paper strips, containing different concentrations of each of two antibiotics, were placed at right angles on an agar plate. After 2 h of diffusion the strips were removed and the plate was inoculated with bacteria. The FCC index was calculated after overnight incubation. Three combinations of antibiotics were studied: trimethoprim-sulphamethoxazole, tobramycin-cefazolin and vancomycin-rifampicin. Over 80% agreement was obtained between the FCC indices and the FIC indices obtained by the chequerboard microdilution technique. The novel diffusion method thus appears promising and warrants further evaluation.

Anti-Bacterial Agents↗
PubMed1988

Interaction between piperacillin and pefloxacin or amikacin on the selection of resistant mutants of Pseudomonas aeruginosa.

Pseudomonas aeruginosa mutants were selected with piperacillin, pefloxacin, amikacin and the combinations pefloxacin-piperacillin and amikacin-piperacillin. With amikacin and the piperacillin-amikacin combination no mutants were selected. With piperacillin (1-32 x MIC) mutants resistant to carboxypenicillins, ureidopenicillins, monobactam and cephalosporins were selected. With pefloxacin, three different types of mutant were observed which showed different patterns of cross-resistance to pefloxacin, sulphonamides, imipenem, piperacillin and other beta-lactam antibiotics. With the pefloxacin-piperacillin association, mutants similar to one of the types selected by pefloxacin alone and resistant to both of the selective antibiotic were predominantly obtained. No mutants were selected with this combination if one of the antibiotics was used at a concentration equal to its MIC for the wild type strain and the other at concentrations above 4 x MIC. Since the association of piperacillin and pefloxacin was only moderately bactericidal against the predominantly cross-resistant mutant selected, the concentration of these antibiotics may have to be carefully controlled to prevent the emergence of such mutants.

Amikacin↗
PubMed2004

New developments in experimental models of inflammatory bowel disease.

PURPOSE OF REVIEW: To consider new data and directions coming from experimental models of inflammatory bowel diseases. RECENT FINDINGS: Advances are discussed in the areas of microbial-host interactions in the intestine, the role of cytokines like IL-23, chemokines like IP-10, and various costimulatory molecules in disease pathogenesis. Multiple regulatory cells have been identified as well as the mechanisms they use to inhibit pathogenic responses to the microbiota in the intestine. New data is available on how the intestine heals after inflammatory insults. SUMMARY: These data are providing fundamental insights into the pathogenesis of IBD and thus are forming the basis of new therapeutic approaches, many of which will be translated to the clinic in the near future.

Journal Article↗
PubMed2000

Hepatocyte toll-like receptor 2 expression in vivo and in vitro: role of cytokines in induction of rat TLR2 gene expression by lipopolysaccharide.

We and others have demonstrated previously that cytokines, including interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNFalpha), regulate LPS recognition proteins such as CD14 in the liver and on hepatocytes. Based on recent findings that the mammalian homologue of Drosophila Toll participates in LPS signaling, we examined the regulation of Toll-Like Receptor (TLR) gene expression by cytokines in vitro and its distribution in vivo with a focus on the liver as a site of host-microbe interaction. Our results show that IL-1beta and/or TNFalpha participate in the upregulation of TLR2 mRNA levels in hepatocytes. Rats treated concurrently with LPS and antagonists of the IL-1 or TNFalpha receptor demonstrated significantly reduced LPS-induced hepatic expression of TLR2 compared to animals treated with LPS alone. The increase in hepatic TLR2 mRNA expression was associated with enhanced transcription as determined by nuclear run-on analysis. LPS treatment in vivo caused a marked TLR2 mRNA up-regulation in all of the tissues examined, with liver showing the highest expression. The high level of TLR2 expression in the liver may have important implications for pathogen-host interactions or microbial signaling.

Animals↗
PubMed1991

4-Quinolone interactions with gyrase subunit B inhibitors.

In studies which have involved determination of fractional inhibitory concentrations, synergy has been described between the 4-quinolones, which inhibit the A subunit of DNA gyrase, and either coumermycin or novobiocin, which inhibit the B subunit of the same enzyme. In this study, fixed concentrations of ciprofloxacin or ofloxacin were combined with varying concentrations of coumermycin or novobiocin and vice versa in nutrient broth. The bactericidal activities of the different mixtures against either Staphylococcus aureus E3T or S. warneri were determined and found to be less than those of equivalent concentrations of either 4-quinolone alone. The observation that gyrase B subunit inhibitors antagonised the bactericidal activity of 4-quinolones is in accordance with the report previously made by others that ciprofloxacin combined with coumermycin was less effective than ciprofloxacin alone in treating staphylococcal endocarditis in rats. Our results indicate that both inhibitory and bactericidal activity should be taken into account when assessing possible interactions in vivo between 4-quinolones and other antimicrobial agents.

Aminocoumarins↗
PubMed2004

Effect of subinhibitory concentration of piperacillin/tazobactam on Pseudomonas aeruginosa.

Subinhibitory concentrations (sub-MICs) of antibiotics, although not able to kill bacteria, can modify their physico-chemical characteristics and the architecture of their outermost surface and may interfere with some bacterial functions. This study investigated the ability of sub-MIC piperacillin/tazobactam (P/T) to interfere with the bacterial virulence parameters of adhesiveness, cell-surface hydrophobicity, motility, biofilm formation and sensitivity to oxidative stress. Antimicrobial activity against five Pseudomonas aeruginosa clinical isolates, representative of clonal lineages of 96 strains of nosocomial origin, and six control strains (ATCC 27853, PAO1, AK1, MT1562, PT623, PAO1algC) was evaluated in vitro using the NCCLS microdilution method. The effects of sub-MIC on bacterial adhesion and biofilm formation were studied using a modified microtitre plate assay. The relative cell-surface hydrophobicity of P. aeruginosa strains was determined by measuring their ability to adhere to n-hexadecane. P. aeruginosa that had been exposed overnight to P/T and incubated with P/T in the plate were also screened for their ability to swim using flagella and to twitch and for their sensitivity to oxidative stress. The results obtained showed that the impact of sub-MIC P/T on bacterial characteristics was different for the various strains of P. aeruginosa. There was a change in bacterial morphology and hydrophobicity that could explain a significant decrease in adhesion values in all clinical isolates and controls tested, a decrease in biofilm formation, a significant increase in sensitivity to oxidative stress, a significant decrease in flagellum-mediated swimming and a decrease in type IV fimbriae-mediated twitching. The results obtained indicate that sub-MIC P/T interferes with the pathogenic potential of P. aeruginosa.

Anti-Bacterial Agents↗
PubMed2026

Implications of proteome allocation constraints for understanding interbacterial antagonism.

Bacteria live in dense communities where competition influences the composition and, therefore, the function of these communities. Beyond competing for resources, bacteria engage in antagonism by deploying a range of molecular weapon systems to inhibit and kill other bacteria. Investing in antagonism is expected to incur a fitness trade-off, but the nature of this trade-off at the level of molecular physiology remains underexplained. Applying recent advances about the physiological constraints faced by bacterial cells may help us better understand existing studies and design new investigations into interbacterial antagonism. Bacterial cells face two important constraints: a finite amount of protein and a maximum translation speed for ribosomes. As a result, the only way for a cell to grow faster is to allocate more of its finite proteome to synthesizing ribosomes. A cell choosing to attack competitors must therefore allocate some of its limited proteome budget to antagonistic proteins instead of other functions. Conversely, being attacked and resisting the effects of such attacks also require an investment of proteomic resources. The extent to which proteome allocation constraints influence bacterial physiology is not fully understood; consequently, how these constraints influence interbacterial antagonism has not been investigated. Here, I will discuss how proteome allocation constraints can re-contextualize our existing understanding of the costs of both deploying and resisting attacks and how investigation of these constraints may further our understanding of interbacterial antagonism.

Proteome↗
PubMed2003

Gene cloning and characterization of VcrM, a Na+-coupled multidrug efflux pump, from Vibrio cholerae non-O1.

We cloned a DNA fragment responsible for drug resistance from chromosome of Vibrio cholerae non-O1. Nucleotide sequence analysis of this fragment revealed the presence of a single open reading frame encoding a protein consisting of 445 amino acid residues. We designated the gene as vcrM. Hydropathy analysis of the deduced amino acid sequence of VcrM suggests the presence of 12 trans-membrane segments. A dendrogram showed that VcrM is a member of the DinF-subfamily within the MATE family of multidrug efflux pumps. Expression of the cloned vcrM gene in drug-hypersensitive Escherichia coli KAM32 cells made them resistant to acriflavine, 4', 6-diamidino-2-phenylindole, Hoechst 33342, rhodamine 6G, tetraphenylphosphonium chloride (TPPCl) and ethidium bromide. Efflux of acriflavine due to VcrM was dependent on Na+ or Li+. Moreover, Na+ efflux was observed with VcrM when TPPCl was added to Na+-loaded cells. Therefore, we conclude that VcrM is a Na+/drug antiporter-type multidrug efflux pump.

Acriflavine↗
PubMed2003

Two different mechanisms are involved in the extremely high-level benzalkonium chloride resistance of a Pseudomonas fluorescens strain.

A Pseudomonas fluorescens strain, PFRB, which we previously isolated as a contaminant in a batch of benzalkonium chloride (BAC) stock solution, exhibits high-level resistance, not only to BAC, but also to other cationic surfactants belonging to disinfectants classified as quaternary ammonium compounds (QACs). In this study, we analyzed the resistance mechanism of the strain to BAC and other disinfectants. We obtained results suggesting that two different mechanisms, reduced adsorption of BAC to the cell surface and an energy-dependent mechanism which is most probably an efflux system, were implicated in the high-level resistance to BAC. Reduced adsorption of BAC is likely due to the decreased negative cell surface charge of the strain. The putative efflux system seems to be unique in that it excretes only a certain range of cationic membrane-acting disinfectants belonging to QACs.

Adsorption↗