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At least 505 records · Page 28Linked to original sources
PubMed1993

Proteolytic enzymes: a new treatment strategy for prosthetic infections?

Among the different mechanisms of bacterial resistance to antimicrobial agents that have been studied, biofilm formation is one of the most widespread. This mechanism is frequently the cause of failure in the treatment of prosthetic device infections, and several attempts have been made to develop molecules and protocols that are able to inhibit biofilm-embedded bacteria. We present data suggesting the possibility that proteolytic enzymes could significantly enhance the activities of antibiotics against biofilms. Antibiotic susceptibility tests on both planktonic and sessile cultures, studies on the dynamics of colonization of 10 biofilm-forming isolates, and then bioluminescence and scanning electron microscopy under seven different experimental conditions showed that serratiopeptidase greatly enhances the activity of ofloxacin on sessile cultures and can inhibit biofilm formation.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2003

In vitro drug interaction modeling of combinations of azoles with terbinafine against clinical Scedosporium prolificans isolates.

The in vitro interaction between terbinafine and the azoles voriconazole, miconazole, and itraconazole against five clinical Scedosporium prolificans isolates after 48 and 72 h of incubation was tested by a microdilution checkerboard (eight-by-twelve) technique. The antifungal effects of the drugs alone and in combination on the fungal biomass as well as on the metabolic activity of fungi were measured using a spectrophotometric method and two colorimetric methods, based on the lowest drug concentrations showed 75 and 50% growth inhibition (MIC-1 and MIC-2, respectively). The nature and the intensity of the interactions were assessed using a nonparametric approach (fractional inhibitory concentration [FIC] index model) and a fully parametric response surface approach (Greco model) of the Loewe additivity (LA) no-interaction theory as well as a nonparametric (Prichard model) and a semiparametric response surface approaches of the Bliss independence (BI) no-interaction theory. Statistically significant synergy was found between each of the three azoles and terbinafine in all cases, although with different intensities. A 27- to 64-fold and 16- to 90-fold reduction of the geometric mean of the azole and terbinafine MICs, respectively, was observed when they were combined, resulting in FIC indices of <1 to 0.02. Using the MIC-1 higher levels of synergy were obtained, which were more consistent between the two incubation periods than using the MIC-2. The strongest synergy among the azoles was found with miconazole using the BI-based models and with voriconazole using the LA-based models. The synergistic effects both on fungal growth and metabolic activity were more potent after 72 h of incubation. Fully parametric approaches in combination with the modified colorimetric method might prove useful for testing the in vitro interaction of antifungal drugs against filamentous fungi.

Antifungal Agents↗
PubMed1981

Syntrophic Association by Cocultures of the Methanol- and CO(2)-H(2)-Utilizing Species Eubacterium limosum and Pectin-Fermenting Lachnospira multiparus During Growth in a Pectin Medium.

Lachnospira multiparus grew very well in an anaerobic 0.2% pectin medium, whereas Eubacterium limosum, which utilizes methanol, H(2)-CO(2), and lactate, did not. Cocultures of the two species grew at a somewhat more rapid growth rate than did L. multiparus alone and almost doubled the amount of growth as measured by optical density. In model experiments with cultures transferred once a day with a 2-day retention time, L. multiparus produced mainly acetate, methanol, ethanol, formate, lactate, CO(2), and H(2) from pectin. The coculture produced one-third more acetate, and butyrate and CO(2) were the only other significant end products. The results are discussed in relationship to microbial metabolic interactions and interspecies hydrogen transfer.

Journal Article↗
PubMed2003

Carbon source-induced modifications in the mycolic acid content and cell wall permeability of Rhodococcus erythropolis E1.

The influence of the carbon source on cell wall properties was analyzed in an efficient alkane-degrading strain of Rhodococcus erythropolis (strain E1), with particular focus on the mycolic acid content. A clear correlation was observed between the carbon source and the mycolic acid profiles as estimated by high-performance liquid chromatography and mass spectrometry. Two types of mycolic acid patterns were observed after growth either on saturated linear alkanes or on short-chain alkanoates. One type of pattern was characterized by the lack of odd-numbered carbon chains and resulted from growth on linear alkanes with even numbers of carbon atoms. The second type of pattern was characterized by mycolic acids with both even- and odd-numbered carbon chains and resulted from growth on compounds with odd-numbered carbon chains, on branched alkanes, or on mixtures of different compounds. Cellular short-chain fatty acids were twice as abundant during growth on a branched alkane (pristane) as during growth on acetate, while equal amounts of mycolic acids were found under both conditions. More hydrocarbon-like compounds and less polysaccharide were exposed at the cell wall surface during growth on alkanes. Whatever the substrate, the cells had the same affinity for aqueous-nonaqueous solvent interfaces. By contrast, bacteria displayed completely opposite susceptibilities to hydrophilic and hydrophobic antibiotics and were found to be strongly stained by hydrophobic dyes after growth on pristane but not after growth on acetate. Taken together, these data show that the cell wall composition of R. erythropolis E1 is influenced by the nutritional regimen and that the most marked effect is a radical change in cell wall permeability.

Acetates↗
PubMed2006

The C-terminal hydrophobic domain of hepatitis C virus RNA polymerase NS5B can be replaced with a heterologous domain of poliovirus protein 3A.

Replication of the plus-stranded RNA genome of hepatitis C virus (HCV) occurs in a membrane-bound replication complex consisting of viral and cellular proteins and viral RNA. NS5B, the RNA polymerase of HCV, is anchored to the membranes via a C-terminal 20-amino-acid-long hydrophobic domain, which is flanked on each side by a highly conserved positively charged arginine. Using a genotype 1b subgenomic replicon (V. Lohmann, F. Korner, J. O. Koch, U. Herian, L. Theilmann, and R. Bartensclager, Science 285:110-113, 1999), we determined the effect of mutations of some highly conserved residues in this domain. The replacement of arginine 570 with alanine completely abolished the colony-forming ability by the replicon, while a R591A change was found to be highly detrimental to replication, viability, and membrane binding by the mutant NS5B protein. Mutations of two other highly conserved amino acids (L588A and P589A) reduced but did not eliminate colony formation. It was of interest, if specific amino acid residues play a role in membrane anchoring of NS5B and replication, to determine whether a complete exchange of the NS5B hydrophobic domain with a domain totally unrelated to NS5B would ablate replication. We selected the 22-amino-acid-long hydrophobic domain of poliovirus polypeptide 3A that is known to adopt a transmembrane configuration, thereby anchoring 3A to membranes. Surprisingly, either partial or full replacement of the NS5B hydrophobic domain with the anchor sequences of poliovirus polypeptide 3A resulted in the replication of replicons whose colony-forming abilities were reduced compared to that of the wild-type replicon. Upon continued passage of the replicon in Huh-7 cells in the presence of neomycin, the replication efficiency of the replicon increased. However, the sequence of the poliovirus polypeptide 3A hydrophobic domain, in the context of the subgenomic HCV replicon, was stably maintained throughout 40 passages. Our results suggest that anchoring NS5B to membranes is necessary but that the amino acid sequence of the anchor per se does not require HCV origin. This suggests that specific interactions between the NS5B hydrophobic domain and other membrane-bound factors may not play a decisive role in HCV replication.

Amino Acid Substitution↗
PubMed2002

Bactericidal effect of gentamicin-induced membrane vesicles derived from Pseudomonas aeruginosa PAO1 on gram-positive bacteria.

Previous studies have shown that gentamicin-induced membrane vesicles (g-MVs) from Pseudomonas aeruginosa PAO1 possess both the antibiotic (gentamicin) and a potent peptidoglycan hydrolase (PGase; autolysin) that is effective in killing gram-negative pathogens. This present study evaluated the therapeutic potential of g-MVs against four gram-positive bacteria. Bactericidal assays and electron microscopy of thin sections revealed that Bacillus subtilis 168 and Staphylococcus aureus D2C were susceptible to killing mediated by g-MVs, Listeria monocytogenes ATCC 19113 was slightly susceptible, whereas Enterococcus hirae ATCC 9790 was unaffected. g-MVs were generally more effective against the bacteria than was soluble gentamicin, suggesting they could have more killing power than natural membrane vesicles containing no antibiotic. Electron microscopy and hydrophobic interaction chromatography showed that more membrane vesicles (MVs) initially attached to B. subtilis (hydrophilic) than to predominantly hydrophobic E. hirae, L. monocytogenes, and S. aureus. Zymograms containing murein sacculi as an enzyme substrate illustrated that all organisms except E. hirae were sensitive to the 26-kDa autolysin to varying degrees. Peptidoglycan O-acetylation did not influence susceptibility to MV-mediated lysis. Though not universally effective, the g-MV delivery system remains a promising therapeutic alternative for specific gram-positive infections.

Anti-Bacterial Agents↗
PubMed2003

Effect of antibiotics on cell surface hydrophobicity of bacteria causing orthopedic wound infections.

BACKGROUND: Despite antibiotic prophylaxis and treatment, the incidence of wound infections in orthopedic surgery is significant. Postoperative wound infection is a multifactorial process, which can be modified by several bacterial factors. Cell surface hydrophobicity of bacteria is a very important physicochemical feature, which has a great influence on the ability of bacteria to adhere to the surface of host cells or medical implants. METHODS: In this study, the hydrophobic properties of thirteen bacterial strains (coagulase-negative staphylococci, Staphylococcus aureus and Pseudomonas aeruginosa) isolated from patients with postoperative deep wound infections following orthopedic procedures were determined by the salt aggregation test. Results were compared to the hydrophobicity of three Hungarian standard bacterial strains. The modifying effect of four antibiotics (cefuroxime, cefotaxime, amoxicillin combined with clavulanic acid and amikacin)--applied most often in our Department for prophylaxis and treatment of patients--were analyzed. RESULTS: The cell surface hydrophobicity of certain strains showed considerable changes after antibiotic treatment. These alterations indicated the decrease in hydrophobicity. Supra-inhibitory concentrations (2x minimum inhibitory concentrations, MIC) of the antibiotics were able to induce more frequent alterations in hydrophobicity than sub-inhibitory (0.5x MIC) levels. CONCLUSIONS: Alterations in cell surface hydrophobicity caused by antibiotics can modify the adhesion process and thus the pathogenicity of bacterial strains. These changes should be taken into consideration in the management of proper antibiotic prophylaxis and in the treatment of orthopedic patients.

Anti-Bacterial Agents↗
PubMed1984

A possible role of intestinal mucin in the pathophysiology of intestinal strangulation obstruction. Consequences of tracing a clinical observation.

In intestinal strangulation obstruction, the pathophysiology is created by factors deriving from the host as well as from the intestinal flora. This article has focused upon the importance of one host-derived factor, i.e. intestinal mucin. Based upon a long series of in vitro and in vivo experiments utilizing germfree as well as conventional animals, it is concluded that intestinal mucin plays a major role in triggering a pathological plasma proteolysis, thereby interacting with microbial products (as endotoxin) in creating the whole variety of serious symptoms found in this situation.

Animals↗
PubMed1979

A rat model of chronic respiratory infection with Pseudomonas aeruginosa.

Chronic, nonlethal, pulmonary infection of rats by Pseudomonas aeruginosa can be initiated by intratracheal inoculation of 10(4) bacteria enmeshed in agar beads. The number of bacteria recoverable from the lung increased to approximately 10(6) within 3 days and remained at that number during 35 days of observation. Histologic examination of the infected lungs revealed lesions resembling those seen in lung tissue of humans with acute or chronic nonbacteremic, Pseudomonas aeruginosa pneumonia, including the presence of goblet-cell hyperplasia, focal areas of necrosis, and acute and chronic inflammatory infiltrate. This model should be useful for investigating the interactions between microbial virulence factors and host defense mechanisms.

Animals↗
PubMed1994

Lectin-mediated interactions of surfactant protein D with alveolar macrophages.

Surfactant protein D (SP-D) is a calcium-dependent carbohydrate-binding protein that is secreted into the pulmonary airspaces by type II epithelial and Clara cells. Previous studies have shown that SP-D can bind to specific surfactant phospholipids and to glycoconjugates associated with the surface of various microorganisms, consistent with possible roles in surfactant metabolism and pulmonary host defense. We now describe specific saccharide-mediated interactions of SP-D with alveolar macrophages in lung tissue and in vitro. Biotinylated rat SP-D showed specific binding to alveolar macrophages in sections of rat lung; this labeling was inhibited by competing saccharides or EDTA. In addition, the binding of 125I-SP-D to isolated alveolar macrophages in the presence of calcium was time-dependent, saturable, and reversible and was preferentially inhibited by known monosaccharide and disaccharide ligands for SP-D. Scatchard analysis gave an apparent single class of binding sites with a Kd = 1.4 x 10(-6) M. We speculate that the multivalent structure of SP-D mediates bridging interactions between microbial glycoconjugates or surfactant phospholipids and specific glycosylated ligands expressed on the surface of phagocytic cells.

Acetylglucosamine↗
PubMed2003

Role of the MyD88 transduction signaling pathway in endothelial activation by antiphospholipid antibodies.

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by the persistent presence of antiphospholipid antibodies (aPLs) and recurrent thrombosis or fetal loss. The thrombophilic state has been partially related to the induction of a proinflammatory and procoagulant endothelial cell (EC) phenotype induced by anti-beta(2)-glycoprotein I (beta(2)-GPI) antibodies that bind beta(2)-GPI expressed on the EC surface. Anti-beta(2)-GPI antibody binding has been shown to induce nuclear factor-kappa B (NF-kappa B) translocation leading to a proinflammatory EC phenotype similar to that elicited by interaction with microbial products (lipopolysaccharide [LPS]) and proinflammatory cytokines (interleukin 1 beta [IL-1 beta], tumor necrosis factor alpha [TNF-alpha]). However, the upstream signaling events are not characterized yet. To investigate the endothelial signaling cascade activated by anti-beta(2)-GPI antibodies, we transiently cotransfected immortalized human microvascular endothelial cells (HMEC-1) with dominant-negative constructs of different components of the pathway (Delta TRAF2, Delta TRAF6, Delta MyD88) together with reporter genes (NF-kappa B luciferase and pCMV-beta-galactosidase). Results showed that both human anti-beta(2)-GPI IgM monoclonal antibodies as well as polyclonal affinity-purified anti-beta(2)-GPI IgG display a signaling cascade comparable to that activated by LPS or IL-1. Delta TRAF6 and Delta MyD88 significantly abrogate antibody-induced as well as IL-1- or LPS-induced NF-kappa B activation, whereas Delta TRAF2 (involved in NF-kappa B activation by TNF) does not affect it. Moreover, anti- beta(2)-GPI antibodies and LPS followed the same time kinetic of IL-1 receptor-activated kinase (IRAK) phosphorylation, suggesting an involvement of the toll-like receptor (TLR) family. Our findings demonstrate that anti-beta(2)-GPI antibodies react with their antigen likely associated to a member of the TLR/IL-1 receptor family on the EC surface and directly induce activation.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

Synthesis, characterization, and antifungal studies of transition metal complexes of omega-bromoacetoacetanilide isonicotinylhydrazone.

Isonicotinic acid hydrazide or isonicotinylhydrazide, commonly known as isoniazid, is an antibacterial agent that has been used to treat tuberculosis. It interacts with microbial cell walls. Schiff's bases or anils are the compounds having >C=N-N< linkages, which have immense applications as catalysts, stabilizers, pigments, dyes, and drugs. They have good ability to form chelates with many metal ions. Isoniazid can form Schiff's bases with diketones such as acetoacetanilide. Acetoacetanilide isonicotinylhydrazone and its metal chelates exhibit anticancer activity. Our studies on N-methylacetoacetanilide isonicotinylhydrazone and its metal chelates revealed that they are active against pathogenic fungal strains. Hence, it is worthwhile to synthesize new complexes of ligands having different substituents on the acetoacetanilide moiety. We synthesized five new metal chelates of omega-bromoacetoacetanilide isonicotinylhydrazone. The ligand behaved as a tridentate monoanion or as a tridentate dianion in the complexes. These compounds were characterized mainly by elemental analysis; conductivity measurements; and electronic, infrared, and nuclear magnetic resonance spectral studies. We also carried out antifungal studies of these compounds against four selected pathogenic fungal strains using a cup-plate technique. Both the ligand and its metal chelates were active against all fungal strains investigated. However, the chelates were found to be more active than the ligand.

Antifungal Agents↗
PubMed2006

Anti-neutrophil cytoplasmic autoantibodies: a renewed paradigm in periodontal disease pathogenesis?

In the past, various models including the autoimmunity model have been proposed to explain the pathogenesis of periodontal diseases. The aim of this review is to introduce the pathogenic role of anti-neutrophil cytoplasmic autoantibodies (ANCAs) in various autoimmune diseases and compare these conditions with periodontal disease to elucidate common pathogenic mechanisms. Also, a novel model to explain the pathogenesis of periodontal disease based on the concept of ANCA-associated autoimmunity is proposed. This encompasses a wide array of biochemical mediators that range from direct and indirect initiators of ANCA production and eventual release of proinflammatory mediators and free radicals, all of which have been implicated in periodontal tissue destruction in the past. In addition, specific links between the typical ANCA-associated diseases and periodontal disease are discussed. Finally, a new paradigm in the periodontal disease-associated destruction is proposed that includes the currently accepted mechanism, namely, the genetic-microbial-host interactions.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2003

Factors determining the efficacy of alpha-helical antimicrobial peptides.

A database of alpha-helical antimicrobial peptides (AMP) was established and their minimum inhibitory concentrations (MIC) were compared with their physiochemical characteristics in an attempt to establish those features that determine efficacy. There is no significant difference in AMP sensitivity between Gram-positive and Gram-negative bacteria but fungi did require higher concentrations to achieve the same degree of growth inhibition. For antibacterial peptides there appears to be a positive correlation between MIC and hydrophobic arc size and a negative correlation between MIC and net charge.

Animals↗
PubMed1996

Immunohistochemical characterization of lymphocyte subsets in chronic adult periodontitis.

It is well known that interactions between microbial dental plaque and the host immune system play a major role in the etiopathogenesis of periodontal disease. The aim of the present study was to analyze the phenotypic properties of gingival T lymphocytes and subsets in patients with chronic inflammatory adult periodontitis (AP) showing various degrees of inflammation and to relate the results to the immunopathogenesis of AP. Gingival biopsies were obtained from patients aged between 26 and 52 yr who were grouped according to gingival index scores (GI) of 1, 2, and 3. Using immunohistochemical techniques, T cells (CD2+), T-helper cells (CD4+) and T-suppressor cells (CD8+) were identified in three well-defined areas of the biopsy samples. Moreover, peripheral blood was collected from the same patients, and relative counts of B cells (CD19+), HLA-DR+ cells and IL-2R+ cells as well as CD3+, CD4+, CD8+ cells were determined using three color flow cytometry. While the blood results were found to be within the normal ranges, the relative counts of CD4+ cells showed statistically significant decreases as the GI score increased. Similarly, the CD4+/CD8+ ratio also decreased. Moreover, gingival T lymphocyte and subset counts appeared to be related to the severity of gingival inflammation. Particularly, CD4+ cells showed a significant increase with the GI score. Furthermore, the CD4+/CD8+ ratio beneath the pocket epithelium was apparently correlated with increasing GI score (p < 0.05). The cytotoxic effect of CD8+ cells seems to be more prominent at the local level while the suppressor effect is more active systematically. This means that the price of systemic protection appears to be local destruction.

Adult↗
PubMed1993

Xylitol and the bactericidal effect of chlorhexidine and fluoride on Streptococcus mutans and Streptococcus sanguis.

The present study was made to investigate the effect of xylitol on the bactericidal and bacteriostatic action of chlorohexidine diacetate (CHX) and sodium fluoride (F) in ATCC strains of Streptococcus mutans and S. sanguis. Standardized bacterial cell suspensions were used in tests for bactericidal effect and for inhibition of growth and sucrose fermentation. The results showed no interference of xylitol with the antibacterial effect of CHX and F combinations. Xylitol did not show any additive effect either but appeared inert in the combinations used.

Analysis of Variance↗
PubMed1991

Antibacterial effects of zinc oxide, rosin, and resin acids with special reference to their interactions.

The growth inhibiting capacity of zinc oxide combined with ordinary rosin (Portuguese rosin), abietic acid or dehydroabietic acid was studied using two different methods. To mimic the actual treatment of wounds, circular tapes or sensitivity discs were placed on Müller-Hinton-agar plates that had been seeded with various facultative aerobic bacteria, and the zones of inhibition were measured. The agar dilution method was used to measure the minimum inhibitory concentration (MIC). Inhibition of growth was restricted to Gram-positive facultative aerobic bacteria for the individual substances zinc oxide, Portuguese rosin, or resin acids, as well as for combinations of these. In general the combination of zinc oxide and dehydroabietic acid was a more potent antibacterial substance than the corresponding combination of zinc with rosin or abietic acid. These combinations commonly had synergistic antibacterial effects.

Abietanes↗
PubMed1998

Free radicals in viral pathogenesis: molecular mechanisms involving superoxide and NO.

The importance of free radical molecular species in the pathogenesis of various viral diseases has been increasingly recognized in recent years. Oxygen radicals such as superoxide (O2-) and hydroxyl radical (.OH) have been implicated as possible pathogenic molecules in viral disease pathogenesis. Much attention has been given to another simple inorganic radical [nitric oxide (NO)] in the host's defense mechanism and pathogenesis of virus infection. The NO synthesis pathway, in particular, the inducible isoform of NO synthase (iNOS), is expressed in different viral diseases via induction of proinflammatory cytokines such as interferon-gamma. iNOS produces an excessive amount of NO for a long time compared with other constitutive isoforms of NOS (i.e., neuronal NOS and endothelial NOS). Recent studies indicate that NO and O2- are produced in excess during the host's defense responses against various intruding microbes. Reactive nitrogen oxide species such as peroxynitrite (ONOO-) and NOx (NO2 and N2O3) are produced in biological systems through the reaction of NO with either O2- or O2. Among these reactive nitrogen species, ONOO- and its biological actions are of considerable interest in that ONOO- causes oxidation and nitration of amino acid residues of proteins and guanine of DNA, lipid peroxidation, and DNA cleavage. Because the ONOO- is formed via a diffusion-limited fast reaction of NO and O2-, it may be a dominant nitrogen oxide species during the host's defense reactions, when both NO and O2- are produced in excess. Thus, understanding the role of NO and oxygen radical generation in virus infections will provide insight into not only viral pathogenesis but also the host-pathogen interaction in microbial infections at a molecular level.

Animals↗