FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2107016911> ?p ?o ?g. }

• W2107016911 endingPage "1357" @default.
• W2107016911 startingPage "1349" @default.
• W2107016911 abstract "The leading cause of mortality in patients with cystic fibrosis (CF) is respiratoy failure due in large part to chronic lung infection with Pseudomonas aeruginosa strains that undergo mucoid conversion, display a biofilm mode of growth in vivo and resist the infiltration of polymorphonuclear leukocytes (PMNs), which release free oxygen radicals such as H2O2. The mucoid phenotype among the strains infecting CF patients indicates overproduction of a linear polysaccharide called alginate. To mimic the inflammatory environment of the CF lung, P. aeruginosa PAO1, a typical non-mucoid strain, was grown in a biofilm. This was treated with low levels of H2O2, as if released by the PMNs, and the formation of mucoid variants was observed. These mucoid variants had mutations in mucA, which encodes an anti-σ factor; this leads to the deregulation of an alternative σ factor (σ22, AlgT or AlgU) required for expression of the alginate biosynthetic operon. All of the mucoid variants tested showed the same mutation, the mucA22 allele, a common allele seen in CF isolates. The mucoid mucA22 variants, when compared to the smooth parent strain PA01, produced 2--6-fold higher levels of alginate|ii) exhibited no detectable differences in growth rate|iii) showed an unaltered LPS profile|iv) were ~72% reduced in the amount of inducible-β-lactamase and (v) secreted little no LasA protease and only showed 44% elastase activity. A characteristic ~54 kDa protein associated with alginate overproducing strains was identified as AlgE (Alg76) by N-terminal sequence analysis. Thus, the common phenotype of the mucoid variants, which included a genetically engineered mucA22 mutant, suggested that the only mutation incurred as a result of H2O2 treatment was in mucA. When a P. aeruginosa biofilm was repeatedly expose to activated PMNs in vitro, mucoid variants were also observed, mimicking in vivo observations. Thus, PMNs and their oxygen by-products may cause P. aeruginosa to undergo the typical adaptation to the intractable mu- coid form in the CF lung. These findings indicate that gene activation in bacteria by toxic oxygen radicals, similar to that found in plants and mammalian cells, may serve as a defence mechanism for the bacteria. This suggests that mucoid conversion is a response to oxygen radical exposure and that this response is mechanism of defence by the bacteria. This is the first report to show that PMNs and their oxygen radicals can cause this phenotypic and genotypic change which is so typical of the intractable form of P. aeruginosa in the CF lung. These findings may provide a basis for the development of anti-oxidant and anti-inflammatory therapy for the early stages of infection in CF patients" @default.
• W2107016911 created "2016-06-24" @default.
• W2107016911 creator A5004969802 @default.
• W2107016911 creator A5004988031 @default.
• W2107016911 creator A5009112406 @default.
• W2107016911 creator A5014012395 @default.
• W2107016911 creator A5025006519 @default.
• W2107016911 creator A5032258415 @default.
• W2107016911 creator A5037360822 @default.
• W2107016911 creator A5046453940 @default.
• W2107016911 creator A5052036637 @default.
• W2107016911 creator A5080481871 @default.
• W2107016911 creator A5086191926 @default.
• W2107016911 creator A5088116014 @default.
• W2107016911 date "1999-06-01" @default.
• W2107016911 modified "2023-10-17" @default.
• W2107016911 title "Mucoid conversion of Pseudomonas aeruginos by hydrogen peroxide: a mechanism for virulence activation in the cystic fibrosis lung" @default.
• W2107016911 cites W1484190159 @default.
• W2107016911 cites W1494351834 @default.
• W2107016911 cites W1497895255 @default.
• W2107016911 cites W1509847467 @default.
• W2107016911 cites W1522816369 @default.
• W2107016911 cites W1530551343 @default.
• W2107016911 cites W1587799736 @default.
• W2107016911 cites W1615357436 @default.
• W2107016911 cites W1757304708 @default.
• W2107016911 cites W1874411209 @default.
• W2107016911 cites W1889683180 @default.
• W2107016911 cites W1891230334 @default.
• W2107016911 cites W1930055114 @default.
• W2107016911 cites W1943943023 @default.
• W2107016911 cites W1967554137 @default.
• W2107016911 cites W1971647449 @default.
• W2107016911 cites W1980004985 @default.
• W2107016911 cites W1994514340 @default.
• W2107016911 cites W2012323946 @default.
• W2107016911 cites W2014417670 @default.
• W2107016911 cites W2016622602 @default.
• W2107016911 cites W2025945102 @default.
• W2107016911 cites W2040107168 @default.
• W2107016911 cites W2044019046 @default.
• W2107016911 cites W2048569323 @default.
• W2107016911 cites W2050499271 @default.
• W2107016911 cites W2052675415 @default.
• W2107016911 cites W2060296327 @default.
• W2107016911 cites W2062460128 @default.
• W2107016911 cites W2066703675 @default.
• W2107016911 cites W2068166540 @default.
• W2107016911 cites W2088587327 @default.
• W2107016911 cites W2089086408 @default.
• W2107016911 cites W2090943591 @default.
• W2107016911 cites W2091187790 @default.
• W2107016911 cites W2099130646 @default.
• W2107016911 cites W2100698746 @default.
• W2107016911 cites W2109588127 @default.
• W2107016911 cites W2125020851 @default.
• W2107016911 cites W2127060683 @default.
• W2107016911 cites W2134912543 @default.
• W2107016911 cites W2145123043 @default.
• W2107016911 cites W2156353316 @default.
• W2107016911 cites W2158937196 @default.
• W2107016911 cites W2163047333 @default.
• W2107016911 cites W2163182389 @default.
• W2107016911 cites W2169380146 @default.
• W2107016911 cites W2169545551 @default.
• W2107016911 cites W2229797209 @default.
• W2107016911 cites W2272680979 @default.
• W2107016911 cites W238623944 @default.
• W2107016911 cites W25592758 @default.
• W2107016911 doi "https://doi.org/10.1099/13500872-145-6-1349" @default.
• W2107016911 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10411261" @default.
• W2107016911 hasPublicationYear "1999" @default.
• W2107016911 type Work @default.
• W2107016911 sameAs 2107016911 @default.
• W2107016911 citedByCount "452" @default.
• W2107016911 countsByYear W21070169112012 @default.
• W2107016911 countsByYear W21070169112013 @default.
• W2107016911 countsByYear W21070169112014 @default.
• W2107016911 countsByYear W21070169112015 @default.
• W2107016911 countsByYear W21070169112016 @default.
• W2107016911 countsByYear W21070169112017 @default.
• W2107016911 countsByYear W21070169112018 @default.
• W2107016911 countsByYear W21070169112019 @default.
• W2107016911 countsByYear W21070169112020 @default.
• W2107016911 countsByYear W21070169112021 @default.
• W2107016911 countsByYear W21070169112022 @default.
• W2107016911 countsByYear W21070169112023 @default.
• W2107016911 crossrefType "journal-article" @default.
• W2107016911 hasAuthorship W2107016911A5004969802 @default.
• W2107016911 hasAuthorship W2107016911A5004988031 @default.
• W2107016911 hasAuthorship W2107016911A5009112406 @default.
• W2107016911 hasAuthorship W2107016911A5014012395 @default.
• W2107016911 hasAuthorship W2107016911A5025006519 @default.
• W2107016911 hasAuthorship W2107016911A5032258415 @default.
• W2107016911 hasAuthorship W2107016911A5037360822 @default.
• W2107016911 hasAuthorship W2107016911A5046453940 @default.
• W2107016911 hasAuthorship W2107016911A5052036637 @default.
• W2107016911 hasAuthorship W2107016911A5080481871 @default.

• next