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PubMed2003

Effects of primary metronidazole and clarithromycin resistance to Helicobacter pylori on omeprazole, metronidazole, and clarithromycin triple-therapy regimen in a region with high rates of metronidazole resistance.

The aim of this study was to investigate the effect of metronidazole resistance (MtzR) and clarithromycin resistance (ClaR) on the eradication rate for omeprazole, clarithromycin, and metronidazole triple-therapy regimen and on the development of posttherapy drug resistance in a region of high rates of MtzR. One hundred ninety-six Helicobacter pylori isolates were recovered from patients with duodenal ulcer, gastric ulcer, or nonulcer dyspepsia during upper endoscopy. The prevalences of MtzR, ClaR, and dual resistance were 37.8%, 13.8%, and 8.7%, respectively. The intention-to-treat eradication rates for metronidazole-susceptible (87.2% vs. 67.6%; P=.001) and clarithromycin-susceptible (86.4% vs. 40.7%; P<.001) strains were significantly higher than the rates for resistant strains. Multiple logistic regression analysis implicated younger age (<40 years old), MtzR, ClaR, and the diagnosis of nonulcer dyspepsia as independent factors that predicted treatment failure. The rates of posttreatment MtzR, ClaR, and dual resistance were 88%, 88%, and 75%, respectively. MtxR and ClaR significantly affected the success of eradication therapy. Posttreatment rates of resistance were high and were related to the presence of pretreatment antibiotic resistance.

Adult↗
PubMed2002

Translocation of integron-associated resistance in a natural system: acquisition of resistance determinants by Inc P and Inc W plasmids from Salmonella enterica Typhimurium DT104.

Salmonella enterica Typhimurium DT104, 961368, a veterinary field isolate that encodes a chromosomal cluster of resistance genes as well as two integrons, was used to study the mobility of resistance cassettes (aadA2 and pse-1) and nonintegron-associated resistance determinants (chloramphenicol and tetracycline). A range of natural plasmids was used as targets for the translocation of resistance. Plasmids that acquired resistance from the DT104 chromosome were segregated by conjugation into Escherichia coli K12. Plasmids R751, R388, and RP4::Tn7 acquired several combinations of resistance determinant (including single cassettes) at frequencies comparable with transposition. RP4 and pOG660 did not acquire any determinants from DT104. Phenotypic and PCR-based analysis of all the transconjugants that were translocated-both cassettes and more complex combinations of determinants-was carried out to determinate the genetic content. Translocation to R751 and R388 was associated with the loss of the indigenous trimethoprim cassette to both plasmids and also acquisition of sulfonamide resistance by R751 and RP4::Tn7, which indicated movement of the 3' terminus of one or both of the DT104 integrons. Sequencing of the R751 transconjugants confirmed these findings and showed that the translocation of streptomycin and ampicillin cassettes was associated with the precise excision of dhfrIIc and orfD cassettes. Furthermore, the translocation of multiple determinants occurred by at least two mechanisms, one of which was likely to involve a circular intermediate analogous to a composite cassette. Instability was detected in some of the transconjugants. The implication of the findings for the dissemination of resistance among clinical isolates is discussed.

Chloramphenicol↗
PubMed1998

Transforming growth factor-beta1 resistance in a thyroid cancer model of tumor necrosis factor-alpha resistance.

We have shown that both tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) inhibit the growth of the human papillary thyroid carcinoma (PTC) cell line, NPA. In previous work, we developed NPA cells that were resistant to the growth suppressive effect of TNF-alpha, called R30, R45, and R60. In this model there were alterations in the p55 and p75 TNF-alpha receptor signaling in the resistant cell lines. In the present work, we studied the action of TGF-beta1 in this PTC cell model. TGF-beta1 (111 pg/mL) inhibited the proliferation of NPA, R30, R45, and the R60 cell lines by 82.8%, 72.1%, 64.2%, and 24.2%, respectively. On Western analysis, TGF-beta1 reduced c-fos content with similar potency in the NPA and R60 cells. In contrast, TNF-alpha reduced c-fos content in the sensitive NPA cells, but failed to do so in the resistant R60 cells. TGF-beta1 reduced p53 content in the NPA but not in the R60 cells, while TNF-alpha did not affect the p53 content in these cells. Furthermore, the resistant cells had a lower baseline p53 content than the NPA cells. The resistant cells had a significantly increased growth rate. Enzyme-linked immunosorbent assay (ELISA) assays with specific antibody against human p53 showed no apparent increase in the mutant form of p53 in the resistant cells. There were also no mutant forms of Ha-Ras, Arg12p21, Val12p21, Asp12p21, and Asp13p21 detected in the resistant cells. The results showed that R30, R45, and R60 cells are partially resistant to TGFbeta1. The mechanisms of action of TNF-alpha and TGF-beta1 differ in their regulation of c-fos and p53 content. The increase in cell proliferation rate is apparently associated with a decrease of p53 content, but not with mutations of p53 or Ha-Ras.

Cell Division↗
PubMed1976

Emergence of gentamicin-resistant bacteria: experience with tobramycin therapy of infections due to gentamicin-resistant organisms.

A computerized system for testing and surveillance of bacterial susceptibility to antibiotics was used in monitoring the emergence of gentamicin-resistant strains of aerobic and facultative gram-negative bacilli at Massachusetts General Hospital since the release of gentamicin for clinical use in 1971. During the period studied, there was a significant increase in the prevalence of gentamicin-resistant bacteria, particularly among Pseudomonas, Acinetobacter (Herellea), and Proteus and, more recently, among Enterobacter and Klebsiella. Most gentamicin-resistant strains of Pseudomonas aeruginosa and Acinetobacter calcoaceticus var. anitratum (Herellea varginicola) retained susceptibility to tobramycin. Of the other gentamicin-resistant organisms, most were also resistant to tobramycin. Twelve patients with infections caused by gentamicin-resistant organisms were treated with tobramycin. All 12 patients were seriously ill, and all but one had failed to respond to previous therapy with gentamicin. Nine patients responded favorably to tobramycin, and six were cured. P. aeruginosa and A. calcoaceticus var. anitratum were most frequently the infecting organisms in these patients. Patients received tobramycin for three to 42 days; no significant drug-related toxicity was noted. These results emphasize the increasing clinical importance of gentamicin-resistant bacteria and suggest that tobramycin may be effective for treatment of some, but not all, infections caused by gentamicin-resistant bacteria.

Acinetobacter↗
PubMed1984

Endocarditis due to methicillin-resistant Staphylococcus aureus in rabbits: expression of resistance to beta-lactam antibiotics in vivo and in vitro.

Whether a strain of methicillin-resistant Staphylococcus aureus susceptible to cephalothin by the disk-diffusion method was also susceptible to cephalothin in vivo was evaluated in the rabbit model of endocarditis. Rabbits with aortic-valve endocarditis due to methicillin-resistant S. aureus that were treated for four days with cephalothin had the same numbers of organisms in vegetations as did untreated rabbits. Treatment with cephalothin caused emergence of a highly resistant subpopulation in aortic-valve vegetations. Organisms highly resistant to cephalothin were also highly resistant to nafcillin. Thus broth-dilution and disk-diffusion tests may not predict therapeutic failure for cephalothin against strains of methicillin-resistant S. aureus. Because of cross-resistances among beta-lactam drugs, these strains should be considered uniformly resistant to this general class of antimicrobial agents, regardless of results from these tests.

Animals↗
PubMed1984

Analysis of plasmids mediating gentamicin resistance in methicillin-resistant Staphylococcus aureus.

Gentamicin-resistance plasmids in methicillin-resistant Staphylococcus aureus isolated from four Australian hospitals have been studied. All the plasmids conferred resistance to gentamicin, tobramycin, kanamycin and all but one conferred resistance to quarternary ammonium compounds. Plasmids which only carried these resistance determinants were ca 15.3 megadaltons and were only found in isolates from one hospital. The most common plasmid was ca 18.0 megadaltons and in addition encoded trimethoprim resistance. Two plasmids, one of ca 19.6 megadaltons and one of ca 28.5 megadaltons were found to carry the penicillinase determinant. However only the larger of these encoded heavy metal ion resistance and was sensitive to quaternary ammonium compounds. EcoR1 analysis indicated that all but the ca 28.5 megadalton plasmid were closely related. The EcoR1 analysis of the ca 28.5 megadalton plasmid indicated that it could have resulted from recombination between a gentamicin resistance determinant and a penicillinase plasmid.

DNA Restriction Enzymes↗
PubMed1986

Antibacterial properties of imipenem with special reference to the activity against methicillin-resistant staphylococci, cefotaxime-resistant Enterobacteriaceae and Pseudomonas aeruginosa.

Imipenem was examined with standardized agar dilution procedures against a wide range of bacteria. Geometric mean MICs against the genera Escherichia, Klebsiella, Enterobacter, Citrobacter and Serratia were 0.1-0.4 mg/l, and Proteus and Providencia spp. were inhibited by 0.25-4 mg/l. Acinetobacter calcoaceticus var. anitratum strains were inhibited by concentrations ranging from 0.12-0.5 mg/l. Methicillin-susceptible staphylococci were highly susceptible to the drug (MICs: less than or equal to 0.03 mg/l) and enterococci were inhibited by 0.25-16 mg/l. Most of the multi-resistant JK corynebacteria were resistant to imipenem. Imipenem was more active than any other beta-lactam against methicillin-resistant staphylococci; this was also demonstrated in a population analysis. Imipenem-resistant minorities in populations, however, were also observed. Cefotaxime-resistant and -intermediate Enterobacter and Citrobacter strains were inhibited by concentrations of 0.5 mg/l or less. No third-generation cephalosporin nor any other beta-lactam showed similarly high activity against these groups of organisms. Among 20 ceftazidime-resistant and 20 ceftazidime-susceptible isolates of Pseudomonas aeruginosa, no strain was resistant and only five ceftazidime-resistant strains were intermediately susceptible (MIC, 8 mg/l) to imipenem.

Anti-Bacterial Agents↗
PubMed2006

Clindamycin-induced enrichment and long-term persistence of resistant Bacteroides spp. and resistance genes.

OBJECTIVES: The aim was to study the long-term consequences of 1 week clindamycin administration regarding selection and persistence of resistance, resistance determinants and diversity of the Bacteroides spp. in the intestinal microflora. METHODS: A total of 1306 Bacteroides isolates were collected from constitutively cultured faecal samples during a 2 year period from eight healthy volunteers. The strains were identified by biochemical and genotyping methods. MIC values were determined by the agar dilution method and presence of resistance genes was screened by real-time PCR. RESULTS: Ecological changes in the intestinal microflora persisting up to 24 months were recorded after a 7 day clindamycin administration to four healthy volunteers. Compared to a control group, not exposed to clindamycin, an enrichment and stabilization of resistant Bacteroides strains and resistance determinants were discovered up to 2 years after clindamycin exposure. CONCLUSIONS: The results indicate that even a short-term antibiotic administration can cause long-term alterations in the commensal microbiota of individual subjects, detectable 2 years after dosing. The recorded selection and persistence of resistant strains and resistance genes, illustrates the importance of increasing our knowledge of the role of the abundant intestinal microbial community as a reservoir for spread of resistance.

Adult↗
PubMed1990

Quantitative genetic tools for insecticide resistance risk assessment: estimating the heritability of resistance.

Quantitative genetic studies of resistance can provide estimates of genetic parameters not available with other types of genetic analyses. Three methods are discussed for estimating the amount of additive genetic variation in resistance to individual insecticides and subsequent estimation of the heritability (h2) of resistance. Sibling analysis and offspring-parent regression permit direct estimates of h2 by comparing the resistance phenotypes of individuals of known relatedness. Threshold trait analyses, performed on data from selection experiments, provide estimates of realized heritability. Procedures are outlined for predicting changes in resistance to insecticides based on h2 estimates. Quantitative genetic theory is examined as it relates to resistance and resistance as a quantitative trait; quantitative genetic methods also are unique in providing estimates of genetic correlations between traits. Comments are included on estimates of genetic correlation between resistance and phenotypic traits (e.g., development time) and how they may be used to predict changes in the genetic aspects of phenology that result from insecticide applications (i.e., to predict how the reproductive capacity of future generations will differ from that of the treated generation).

Analysis of Variance↗
PubMed1990

Isolation of human colon carcinoma cells for resistance to a single interferon associated with cross-resistance to multiple recombinant interferons: alpha, beta, and gamma.

We established variants resistant to human interferon (IFN) from an IFN-sensitive human colon carcinoma cell line and delineated some of the mechanisms for resistance to IFN-mediated cytotoxicity. The parent KM12C cells were incubated for 2 months in medium containing recombinant human IFN-alpha hybrid BBDD (r-IFN-alpha) or recombinant human IFN-gamma (r-IFN-gamma). Surviving variants were designated KM12 alpha R and KM12 gamma R, respectively. KM12 alpha R cells were cross-resistant to the cytostatic and cytolytic effects of r-IFN-alpha, r-IFN-beta, and r-IFN-gamma, whereas KM12 gamma R cells were resistant only to the effects of r-IFN-gamma. The parent and variant cell lines had similar in vitro growth rates and similar tumorigenicity in male BALB/c nude mice, but the mechanisms for resistance to IFNs differed in the two variant lines. The resistance of the cross-resistant KM12 alpha R cell line was not attributable to the loss of specific receptors, because our analyses demonstrated the presence of receptors for IFN-gamma, whereas the KM12 gamma R line lacked specific receptors for IFN-gamma. Northern blot analyses revealed that messenger RNA (mRNA) from the proto-oncogene c-myc was equally expressed in the IFN-sensitive and IFN-resistant cell lines and that treatment with r-IFN-gamma did not alter its expression. Treatment with r-IFN-gamma induced the expression of manganous superoxide dismutase mRNA in KM12C and KM12 alpha R cells, but not in KM12 gamma R cells, confirming that both KM12C and KM12 alpha R cells, but not KM12 gamma R cells, have functional receptors for IFN-gamma.

Blotting, Northern↗
PubMed1993

Differential reversal of lipophilic antifolate resistance in mammalian cells with modulators of the multidrug resistance phenotype.

Chinese hamster ovary (CHO) T19 cells express a stable P-glycoprotein (P-170)-dependent multidrug resistance (MDR) phenotype and display a 24- to 29-fold cross-resistance to the lipophilic antifolates piritrexim (PTX) and trimetrexate (TMTX). We have examined the ability of various modulators of the MDR phenotype to sensitize T19 cells to TMTX and PTX in a clonogenic assay. An almost complete reversal of TMTX resistance in T19 cells was achieved with several modulators of the MDR phenotype whereas only a partial sensitization of T19 cells to PTX was obtained with the most potent modulator. In an attempt to explore the apparent P-170-independent locus of protection against PTX, resistant T19 sublines were isolated after stepwise selection with PTX and TMTX. Thus, T19 cells made resistant to PTX displayed a dramatic decrease in P-170 mRNA levels despite the maintenance of the parental T19 MDR gene amplification, whereas T19 cells selected for TMTX resistance exhibited a further increase in P-170 mRNA levels. Hence, the modulation experiments together with the established lipophilic antifolate-resistant T19 variants suggest that although T19 cells possess a P-170-dependent MDR phenotype and display a similar cross-resistance to TMTX and PTX, the protective pathway need not be necessarily via P-170. Rather, a pathway appears to exist that protects T19 MDR cells from the cytotoxicity of PTX without requiring a P-170 function.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

Chemosensitization and drug accumulation effects of VX-710, verapamil, cyclosporin A, MS-209 and GF120918 in multidrug resistant HL60/ADR cells expressing the multidrug resistance-associated protein MRP.

Overexpression of the multidrug resistance MDR1 gene product P-glycoprotein and/or the multidrug resistance-associated protein MRP confers multidrug resistance to cancer cells. The pipecolinate derivative VX-710 has previously been demonstrated to reverse MDR1-mediated multidrug resistance at concentrations of 0.5-2.5 microM by direct interaction with P-glycoprotein and inhibition of its drug efflux activity. In this study we investigated whether VX-710 as well as four other known MDR1 modulators could also reverse multidrug resistance mediated by MRP. VX-710 at 0.5-5 microM restored senstivity of MRP-expressing HL60/ADR promyelocytic leukemia cells to the cytotoxic action of doxorubicin, etoposide and vincristine. VX-710 was approximately 2-fold more effective than verapamil, MS-209 and CsA in modulating MRP-mediated multidrug resistance, whereas GF120918 had no significant effect. VX-710 was also more effective than verapamil, MS-209 and CsA in restoring the daunorubicin accumulation deficit in HL60/ADR cells and in increasing calcein uptake. A photoaffinity analog of VX-710, [3H]VF-13,159, specifically photo labeled the MRP protein and unlabeled VX-710 inhibited this binding in a concentration-dependent manner. These data suggest that VX-710 is not only a potent modulator of P-glycoprotein-mediated multidrug resistance, but also affects multidrug resistance in MRP-expressing cells and may exert its action, at least in part, by binding directly to MRP.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2003

Establishment of gemcitabine-resistant human pancreatic cancer cells and effect of brefeldin-a on the resistant cell line.

To date, no therapy has been found to which pancreatic cancer responds with the exception of surgical resection in early stages. Recently, gemcitabine has become the standard of care for chemotherapy in those patients with advanced disease. Most pancreatic tumors however, develop resistance to gemcitabine. The aim of this study is to clarify the mechanism of resistance to gemcitabine in human pancreatic cells. Using a cell selection method, a human pancreatic cancer cell line resistant to gemcitabine was established. Cellular proliferation and viability were determined by MTT assay. The cell line with acquired resistance was also found to have cross resistance to fluorouracil. Brefeldin-A (BFA) has been used as a tool for studies of intracellular protein traffic, rather than as an anticancer drug. BFA displays the same effects on wild type cells and those with acquired resistance. Gemcitabine combined with BFA in low doses is significantly more effective than gemcitabine alone against MIA PaCa-2 cell line. Our data suggest that the gemcitabine-resistant and 5-FU-resistant pathways may partially overlap each other. In short, BFA may be used as a modulator of gemcitabine.

Brefeldin A↗
PubMed2001

International perspectives on antiretroviral resistance. Clinical utility of resistance testing: retrospective and prospective data supporting use and current recommendations.

Data from retrospective and prospective studies support use of genotypic and phenotypic resistance assays to guide treatment changes when initial or subsequent antiretroviral regimens fail. Several retrospective studies have shown that response to antiretroviral therapy can be predicted based on genotypic analysis of HIV, with baseline genotypic evidence of resistance predicting virologic failure. Other retrospective analyses demonstrated that phenotypic drug sensitivity correlates with increased viral load suppression, particularly when virus remains sensitive to two or three drugs at initiation of the regimen. Furthermore, prospective studies such as VIRADAPT and Genotype-Assisted Antiretroviral Resistance Testing (GART) have substantiated that drug selection based on genotypic assay results yield superior viral suppression compared with empiric treatment assignment. One additional study suggested significant improvement in short-term virologic outcome when phenotypic testing was used to guide treatment selection. Based on these findings, resistance testing is currently recommended for patients with acute HIV infection, those who have failed one or more antiretroviral regimens, and pregnant women. Although these tests move toward becoming a standard of care, several research questions remain: the long-term benefit of resistance testing is not yet certain, the interpretation of specific genotypic resistance patterns needs to be better defined, and clinical cut-off points for phenotypic resistance need to be established. As these issues continue to be studied, resistance testing likely will prove a reliable tool to help plan successful ART strategies.

Anti-HIV Agents↗
PubMed2004

Antimicrobial resistance patterns (1999-2002) and characterization of ciprofloxacin-resistant Neisseria gonorrhoeae in Korea.

BACKGROUND: Antimicrobial susceptibilities of Neisseria gonorrhoeae were monitored during 4 years. In Korea, ciprofloxacin-resistant N. gonorrhoeae has dramatically increased after recommendation as a therapeutic drug. GOAL: The goal of this study was to determine the resistance patterns and characterize Korean ciprofloxacin-resistant N. gonorrhoeae. STUDY DESIGN: Antimicrobial susceptibilities were performed. PFGE profile and DNA sequencing of gyrA and parC genes were used to characterize the ciprofloxacin-resistant isolates in Korea. RESULTS: Tetracycline, ofloxacin, ciprofloxacin-resistant isolates were increased and among them, the proportion of isolates resistant to ciprofloxacin increased remarkably from 1% in 1999 to 48.8% in 2002. Fifteen different types by PFGE profile were identified. Major alteration type was M12 (67%), which have amino acid substitution in gyrA (S-91-->F, D-95-->G) and parC (S-87-->A). CONCLUSION: We could conclude that resistance for ciprofloxacin was remarkably increased during 4 years. Ciprofloxacin-resistant N. gonorrhoeae was supposed by the spread of several strains that had a small number of origins.

Anti-Bacterial Agents↗
PubMed1988

Vincristine-resistant human cancer KB cell line and increased expression of multidrug-resistance gene.

A multidrug-resistant clone of human cancer KB cells was isolated by stepwise selection on exposure to increasing doses of vincristine. The final clone, VJ-300, obtained after ethylmethane sulfonate mutagenesis showed 400-fold higher resistance to vincristine than did KB cells. Cellular accumulation of vincristine in VJ-300 was decreased to less than one-tenth of that in KB. The cells were also cross-resistant to daunomycin, adriamycin, actinomycin D, colchicine and VP-16. During continuous culturing in the absence of any drug for several months, a different colchicine-resistant and multidrug-resistant clone, KB-C1, reverted almost completely to drug sensitivity, whereas drug resistance in VJ-300 was stably maintained. Amplification of the multidrug-resistance-1 (mdr-1) gene was more than 20-fold in KB-C1, but less than 2-fold in VJ-300. mdr-1 mRNA was, however, expressed in VJ-300 at a rate comparable to KB-C1. Acquisition of high multidrug resistance in VJ-300 might be correlated with both activated transcription of mdr-1 gene and amplification.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Cisplatin-resistant HeLa cells are resistant to apoptosis via p53-dependent and -independent pathways.

Since HeLa cells possess very little functional p53 activity, they could be originally resistant to genotoxic stress-induced apoptosis. Therefore, it is likely that the drug-resistant cells derived from HeLa cells are more resistant to apoptosis. The aim of this study was to determine whether cisplatin-resistant cells derived from HeLa cells have an apoptosis-resistant phenotype. A cisplatin-resistant cell subline, HeLa/CDDP cells, showed a 19-fold resistance to cisplatin compared with the parent cells. The subline showed a collateral sensitivity to paclitaxel. An equitoxic dose (IC50) of cisplatin produced DNA fragmentation in HeLa cells but not in HeLa/CDDP cells. Transfection of wild-type p53 gene enhanced the cytotoxicity of cisplatin and cisplatin-induced apoptosis in HeLa cells but not in HeLa/CDDP cells, although it caused p53 overexpression in both cell lines. The expression of caspase 1 (interleukin-1beta-converting enzyme, ICE) mRNA and the overexpression of bax protein were observed only in HeLa cells. Paclitaxel-induced DNA fragmentation appeared less in HeLa/CDDP cells than in HeLa cells. p53 gene transfection did not affect the extent of DNA fragmentation in either cell line, suggesting that paclitaxel may induce p53-independent apoptosis. These findings suggest that HeLa/CDDP cells may have an acquired phenotype that is resistant to p53-dependent and -independent apoptosis.

Antineoplastic Agents↗
PubMed1999

Isolation of a taxol-resistant Leishmania donovani promastigote mutant that exhibits a multidrug-resistant phenotype.

We raised a strain of Leishmania donovani in the laboratory that was resistant to 500 nM taxol. The IC50 of the wild-type strain for taxol was 35 nM and that of the taxol-resistant strain (T-500) was 1 microM. The T-500 strain exhibited a Mdr phenotype; it was also resistant to other unrelated drugs like vinblastine, adriamycin and the commonly used antimonial drugs pentostam and glucantime. Verapamil (20 nM), a calcium channel blocker, was found to reverse the resistance of T-500 to taxol. Acquired resistance to taxol has been reported to be mediated by alterations involving tubulin in cancer cells. Thus polymerisation assays with tubulin fractions in wild-type versus taxol-resistant cells (T-500) were performed in vitro. The tubulin fraction from T-500 was more resistant to in vitro polymerisation than the tubulin isolated from the wild-type, suggesting that this is one means by which the parasite may acquire resistance to taxol.

Animals↗