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Pseudomonas aeruginosa lipid

LPS with endotoxic properties is not confined to pathogens. Whole cells or cell extracts from commensal organisms often show the same degree of biological activity as similar extracts or killed whole cells from a pathogenic strain. By contrast the potency of lipid A varies with source. Despite the severity of infections caused by them, brucellae and yersiniae possess LPS of relatively low toxicity. Similarly Pseudomonas aeruginosa lipid A is less toxic than that derived from Enterobacteriaceae. This is thought to be a result of the predominance of 12 carbon 3-hydroxy fatty acid substituents... [Pg.166]

Fig. 11.—Chemical structure of the two preponderant lipid A forms of Pseudomonas aeruginosa. (A) Pentaacyl lipid A (major lipid A fraction 75%, w/w). (B) Hexaacyl lipid A (minor lipid A fraction, 25%, w/w). Dashed lines indicate nonstoichiometric a-hydroxylation of 12 0. A lipid A species having 2 mol 12 0(2-OH)/mol lipid A was not detected (77). Fig. 11.—Chemical structure of the two preponderant lipid A forms of Pseudomonas aeruginosa. (A) Pentaacyl lipid A (major lipid A fraction 75%, w/w). (B) Hexaacyl lipid A (minor lipid A fraction, 25%, w/w). Dashed lines indicate nonstoichiometric a-hydroxylation of 12 0. A lipid A species having 2 mol 12 0(2-OH)/mol lipid A was not detected (77).
Moskowitz, S., Ernst, R., Miller, S. PmrAB, a two-component regulatory system of Pseudomonas aeruginosa that modulates resistance to cationic antimicrobial peptides and addition of aminoarabinose to lipid A. J Bacteriol 186 (2004) 575-579. [Pg.119]

Keywords Pseudomonas aeruginosa Cystic fibrosis Lipopolysaccharide Lipid A Chronic infection Antibiotic resistance Innate immunity inflammation... [Pg.241]

Bhat, R., Marx, A., Galanos, C., Conrad, R.S. Structural studies of lipid A from Pseudomonas aeruginosa PAOl occurrence of 4-amino-4-deoxyarabinose. J Bacteriol 172 (1990)... [Pg.251]

Goldman, R.C., Doran, C.C., Kadam, S.K.,Capobianco, J.O. Lipid A precursor from Pseudomonas aeruginosa is completely acylated prior to addition of 3-deoxy-D-manno-octulosonate. J Biol Chem 263 (1988) 5217-5223. [Pg.252]

Karunaratne, D.N., Richards, J.C., Hancock, R.E.W. Characterization of lipid A from Pseudomonas aeruginosa O-antigenic B band lipopolysaccharide by ID and 2D NMR and mass spectral analysis. Arch Biochem Biophys 299 (1992) 368-376. [Pg.252]

Kulshin, V.A., Zahringer, U., Lindner, B., Jager, K.E., Dmitriev, B.A., Rietschel, E.T. Structural characterization of the lipid A component of Pseudomonas aeruginosa wild-type and rough mutant lipopolysaccharides. Eur J Biochem 198 (1991) 697-704. [Pg.252]

Moskowitz, S.M., Bums, J.L., Nguyen, C.D., Hftiby, N., Ernst, R.K., Miller, S.I. Polymyxin resistance and lipid A structure of Pseudomonas aeruginosa isolated from colistin-treated and colistin-naive cystic fibrosis patients. Pediatr Pulmonol Suppl 20 (2000) 272. [Pg.252]

Polymyxin E (colistin) is used in the treatment of serious Gram-negative bacterial infections, particularly those caused by Pseudomonas aeruginosa. It binds tightly to the lipid A component of LPS in the outer membrane of Gram-negative bacteria. The outer leaflet of the membrane structure is distorted, segments of which are released and the permeability barrier is destroyed. The polymyxin mole-... [Pg.218]

Some polymyxins are sold for second-line systemic therapy. Polymyxin B sulfate and colistimethate sodium can be used for intravenous, intramuscular, or intrathecal achninistration, especially for Pseudomonas aeruginosa infections, but also for most other gram-negative organisms, such as those resistant to first-line antibiotics. Nephrotoxicity and various neurotoxicities are common in parenteral, but not in topical, use. Resistance to polymyxins develops slowly, involves mutation and, at least in some bacteria, adaptation, a poorly understood type of resistance that is rapidly lost on transfer to a medium free of polymyxin. Resistance can involve changes in the proteins, the lipopolysaccharides, and lipids of the outer membrane of the cell (52). Polymyxin and colistin show complete cross-resistance. [Pg.149]

Jarvis, F. G., Johnson, M. J. (1949). A glyco-lipid produced by Pseudomonas aeruginosa. Journal of the American Chemical Society. 71, 4121-4126. [Pg.413]

Resistance against ascites tumour development and interferon-inducing activity has been demonstrated in the lipopolysaccharide derived from the protein-lipopolysaccharide complex of Pseudomonas aeruginosa Both the lipid A portion and the covalently linked polysaccharide-protein complex appear to be necessary for inhibition of tumour development, whereas the lipid A with amide-linked fatty acid is suficient to induce the in vitro formation of interferon. The lipopolysaccharide of P. aeruginosa has a more pronounced effect as immunogen, mitogen, and interferon inducer than the lipopolysaccharide of Brucella melitensis, although they have similar toxicity levels. Since lipid A is responsible for most of these activities, the variations may be partially explained by structural differences in the lipopolysaccharides. [Pg.289]

H. Benamara, C. Rihouey, T. Jouenne, S. Alexandre. Impact of the biofihn mode of growth on the inner membrane phospholipid composition and lipid domains in Pseudomonas aeruginosa. Biochimica et Biophysica Acta, Woh 1808, pp. 98-105, 2011. [Pg.120]

Pseudomonas aeruginosa 42A2 was used by Fernandez et al. (2005) for PHA production from oily wastes such as residual waste cooking oil and other lipid wastes the organism accumulated up to 54.6% of PHA. The authors investigated the influence of k a and temperature on PHA productivity and monomer composition. [Pg.98]


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See also in sourсe #XX -- [ Pg.244 ]




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