Evolution of amoxicillin resistance of Helicobacter pylori in vitro: characterization of resistance mechanisms.

Helicobacter pylori is the major cause of peptic ulcers and gastric cancer in humans. Treatment involves a two or three drug cocktail, typically including amoxicillin. Increasing levels of resistance to amoxicillin contribute to treatment failures, and higher levels of resistance are believed to be due to multiple genetic mutations.

Contribution of specific amino acid changes in penicillin binding protein 1 to amoxicillin resistance in clinical Helicobacter pylori isolates.

Amoxicillin is commonly used to treat Helicobacter pylori, a major cause of peptic ulcers, stomach cancer, and B-cell mucosa-associated lymphoid tissue lymphoma. Amoxicillin resistance in H. pylori is increasing steadily, especially in developing countries, leading to treatment failures.

Antibacterial effects of green tea polyphenols on clinical isolates of methicillin-resistant Staphylococcus aureus.

The antibacterial effects of tea polyphenols (TPP) extracted from Korean green tea (Camellia sinensis) against clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA) were evaluated. Characterization of the minimal inhibitory concentration (MIC) of oxacillin for 30 S. aureus strains isolated from patients treated with oxacillin identified 13 strains with an oxacillin MIC >or= 4 microg/mL as methicillin-resistant Staphylococcus aureus (MRSA) (range: 8 to 512 microg/mL), while 17 strains were methicillin-susceptible Staphylococcus aureus (MSSA) (range: 0.

Bacteria and bacterial rRNA genes associated with the development of colitis in IL-10(-/-) mice.

Background: Microorganisms appear to play important yet ill-defined roles in the etiology of inflammatory bowel disease (IBD). This study utilized a novel population-based approach to identify bacteria and bacterial rRNA genes associated with the development of colitis in IL-10(-/-) mice.

Methods: Mice were housed in 2 environments: a community mouse facility where the mice were fed nonsterile chow (Room 3) and a limited access facility where the mice were fed sterile chow (Room 4).

Resistance mechanisms in an in vitro-selected amoxicillin-resistant strain of Helicobacter pylori.

We investigated the beta-lactam resistance mechanism(s) of an in vitro-selected amoxicillin-resistant Helicobacter pylori strain (AmoxR). Our results demonstrated that resistance is due to a combination of amino acid substitutions in penicillin binding protein 1 (PBP1), HopB, and HopC identified in AmoxR, resulting in decreased affinity of PBP1 for amoxicillin and decreased accumulation of penicillin.

Alginate lyase enhances antibiotic killing of mucoid Pseudomonas aeruginosa in biofilms.

Once mucoid (alginate-producing) strains of Pseudomonas aeruginosa have become established in the respiratory tracts of cystic fibrosis patients they can rarely be eliminated by antibiotic treatment alone; we have investigated, in an in vitro biofilm system, the putative role of co-administration of alginate lyase with antibiotic. Biofilms were maintained in continuous flow culture in a medium resembling sputum from CF patients. Antibiotics and/or alginate lyase were added to some of the cultures.

Alginate lyase (AlgL) activity is required for alginate biosynthesis in Pseudomonas aeruginosa.

To determine whether AlgL's lyase activity is required for alginate production in Pseudomonas aeruginosa, an algLdelta::Gm(r) mutant (FRD-MA7) was created. algL complementation of FRD-MA7 restored alginate production, but algL constructs containing mutations inactivating lyase activity did not, demonstrating that the enzymatic activity of AlgL is required for alginate production.

AlgX is a periplasmic protein required for alginate biosynthesis in Pseudomonas aeruginosa.

Alginate, an exopolysaccharide produced by Pseudomonas aeruginosa, provides the bacterium with a selective advantage that makes it difficult to eradicate from the lungs of cystic fibrosis (CF) patients. Previous studies identified a gene, algX, within the alginate biosynthetic gene cluster on the P. aeruginosa chromosome.

Binding of protegrin-1 to Pseudomonas aeruginosa and Burkholderia cepacia.

Background: Pseudomonas aeruginosa and Burkholderia cepacia infections of cystic fibrosis patients' lungs are often resistant to conventional antibiotic therapy. Protegrins are antimicrobial peptides with potent activity against many bacteria, including P. aeruginosa.