Disease relevance of Pseudomonas

• Transposition of Pseudomonas toluene-degrading genes and expression in Escherichia coli [1].
• Colonization of the lungs of cystic fibrosis (CF) patients by the opportunistic bacterial pathogen Pseudomonas aeruginosa is the principal cause of mortality in CF populations [2].
• An epidemiologic investigation found the amphotericin B to be contaminated with Enterobacter agglomerans, Pseudomonas fluorescens, and P aeruginosa [3].
• The airway surface fluid (ASF) from CF xenografts failed to kill Pseudomonas aeruginosa or Staphylococcus aureus [4].
• Eight strains of three genera (Proteus, Escherichia, Pseudomonas) isolated at Boston City Hospital or Institut Pasteur, Paris, showed antagonism of carbenicillin or ampicillin by cephaloridine, cloxacillin, or 6-aminopenicillanic acid [5].

Psychiatry related information on Pseudomonas

• Permissiveness to L. pneumophila was not the consequence of a general defect in the microbicidal capacities because killing of a temperature-sensitive mutant of Pseudomonas aeruginosa was normal in DN PKC-alpha-overexpressing RAW 264.7 clones [6].
• We investigated the in vitro and in vivo effects of a combination of a beta-lactam (ceftazidime) and a beta-lactamase inhibitor (dicloxacillin) to synergistically kill a ceftazidime-resistant variant, Pseudomonas aeruginosa PA-48, which overproduces type Id cephalosporinase constitutively [7].
• The local skin tissue concentration of 50% and 100% gentamicin sulphate, loaded full IPNs (i.e., Ax-1 and Ax-2), was found to be higher (20+/-2mug/g) than the minimum bactericidal concentration for Staphylococcus aureus (1.2mug/g) and Pseudomonas aeruginosa (10mug/g), respectively, for a study time of 60 days [8].
• One death in the limited-spectrum empirical antimicrobial therapy group was due to autopsy-proved disseminated Pseudomonas aeruginosa (blood, peritoneum, lung, and pleural fluid) that was resistant to cefoxitin, and the other was associated with peritonitis due to cefoxitin-resistant Enterobacter cloacae [9].

High impact information on Pseudomonas

• Two Pseudomonas syringae type III effectors inhibit RIN4-regulated basal defense in Arabidopsis [10].
• In Arabidopsis, RPM1 confers resistance against Pseudomonas syringae expressing either of two sequence unrelated type III effectors, AvrRpm1 or AvrB [11].
• The Pto serine/threonine kinase of tomato confers resistance to speck disease by recognizing strains of Pseudomonas syringae that express the protein AvrPto [12].
• In tomato, resistance to Pseudomonas syringae pv. tomato (Pst) strains expressing the avirulence gene avrPto requires the presence of at least two host genes, designated Pto and Prf [13].
• Barnase toxin: a new chimeric toxin composed of pseudomonas exotoxin A and barnase [14].

Chemical compound and disease context of Pseudomonas

• Pseudomonas aeruginosa exotoxin A [15].
• Pseudobacteremia caused by povidone-iodine solution contaminated with Pseudomonas cepacia [16].
• Here we report the directed evolution of the P450 from Pseudomonas putida to create mutants that hydroxylate naphthalene in the absence of cofactors through the 'peroxide shunt' pathway with more than 20-fold higher activity than the native enzyme [17].
• Some bacteria such as Pseudomonas aeruginosa synthesize SA using isochorismate synthase (ICS) and pyruvate lyase [18].
• Host defense against Pseudomonas aeruginosa requires ceramide-rich membrane rafts [19].

Biological context of Pseudomonas

• Exploitation of syndecan-1 shedding by Pseudomonas aeruginosa enhances virulence [20].
• Phagocytosis of unopsonized Pseudomonas aeruginosa by murine macrophages is a two-step process requiring glucose [21].
• Lipid A-free polysaccharide (PS) isolated from Pseudomonas aeruginosa immunotype 5 lipopolysaccharide (LPS) was covalently coupled to toxin A via reductive amination [22].
• RepA is the DNA replication initiator protein of the Pseudomonas plasmid pPS10 [23].
• The crystal structure for the negative regulator (AmiC) of the amidase operon from Pseudomonas aeruginosa has been solved at a resolution of 2.1 A [24].

Anatomical context of Pseudomonas

• In this study, we determined whether the binding of specific Pseudomonas gene products (pilin, flagellin) to their receptors on respiratory epithelial cells would result in production of the neutrophil chemoattractant IL-8 [25].
• Diverse Pseudomonas aeruginosa gene products stimulate respiratory epithelial cells to produce interleukin-8 [25].
• These antibodies were covalently linked to either Pseudomonas exotoxin (PE) or ricin A chain (RTA), and the conjugates were tested against five ovarian cancer cell lines (OVCAR-2, -3, -4, -5; A1847) [26].
• Interaction of the Pseudomonas aeruginosa secretory products pyocyanin and pyochelin generates hydroxyl radical and causes synergistic damage to endothelial cells. Implications for Pseudomonas-associated tissue injury [27].
• Proteinases of Pseudomonas aeruginosa evoke mucin release by tracheal epithelium [28].

Gene context of Pseudomonas

• Here we show that lactoferrin, a ubiquitous and abundant constituent of human external secretions, blocks biofilm development by the opportunistic pathogen Pseudomonas aeruginosa [29].
• These C5a-receptor-deficient mice challenged with sublethal inocula of Pseudomonas become superinfected with secondary bacterial strains [30].
• In cystic fibrosis (CF), defective function of the cystic fibrosis transmembrane conductance regulator (CFTR) in airway epithelial cells and submucosal glands results in chronic pulmonary infection with Pseudomonas aeruginosa [31].
• Neither bacterial strain induced inflammation in wild-type mice, and germ-free and Pseudomonas fluorescens-monoassociated interleukin 10 -/- mice remained disease free [32].
• Previously, we (Kounnas, M.Z., R.E. Morris, M.R. Thompson, D.J. FitzGerald, D.K. Strickland, and C.B. Saelinger. 1992. J. Biol. Chem. 267:12420-12423) [corrected] showed that Pseudomonas exotoxin (PE) could bind immobilized LRP [33].

Analytical, diagnostic and therapeutic context of Pseudomonas

• Bronchoalveolar lavages were performed upon 13 patients with CF, 7 patients with chronic bronchitis characterized by recurrent Pseudomonas infections, and 4 normal volunteers [34].
• Further, a bis-thioether ferrous H93G model for bis-methionine ligation, as found in Pseudomonas aeruginosa bacterioferritin heme protein, is described [35].
• Immunosuppression has also been observed in animals immunized with multiple doses (10 mg x 7 d) of Pseudomonas exotoxin and treated with DSG at a dose of 5 mg/kg for 21 days [36].
• Because IL-4 cytotoxin comprised of a circularly permutated IL-4 and a mutated form of Pseudomonas exotoxin [IL4(38-37)-PE38KDEL] is cytotoxic to IL-4R-expressing cells, we tested whether primary GBM explant cell cultures are sensitive to IL-4 cytotoxin [37].
• This gene therapy strategy exploits the toxic pro-oxidant property of methylselenol, which is released from selenomethionine (SeMET) by cancer cells with the adenoviral-delivered methionine alpha,gamma-lyase (MET) gene cloned from Pseudomonas putida [38].

References