2009
Role of LecA and LecB Lectins in Pseudomonas aeruginosa-Induced Lung Injury and Effect of Carbohydrate Ligands
CHEMANI, Chanez, Anne IMBERTY, Sophie DE BENTZMANN, Maud PIERRE, Michaela WIMMEROVÁ et. al.Základní údaje
Originální název
Role of LecA and LecB Lectins in Pseudomonas aeruginosa-Induced Lung Injury and Effect of Carbohydrate Ligands
Název česky
Uloha lektinu LecA a LecB v poskozeni plic vyvolanych Pseudomonas aeruginosa a efekt ligandu na bazi sacharidu
Název anglicky
Role of LecA and LecB Lectins in Pseudomonas aeruginosa-Induced Lung Injury and Effect of Carbohydrate Ligands
Autoři
CHEMANI, Chanez (250 Francie), Anne IMBERTY (250 Francie), Sophie DE BENTZMANN (250 Francie), Maud PIERRE (250 Francie), Michaela WIMMEROVÁ (203 Česká republika, garant), Benoit P. GUERY (250 Francie) a Karine FAURE (250 Francie)
Vydání
INFECTION AND IMMUNITY, The American Society for Microbiology, 2009, 0019-9567
Další údaje
Jazyk
čeština
Typ výsledku
Článek v odborném periodiku
Obor
10610 Biophysics
Stát vydavatele
Norsko
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 4.205
Kód RIV
RIV/00216224:14310/09:00029451
Organizační jednotka
Přírodovědecká fakulta
UT WoS
000265279900037
Klíčová slova anglicky
lectin; infection;preudomonas aeruginosa
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 24. 8. 2009 16:15, prof. RNDr. Michaela Wimmerová, Ph.D.
V originále
Pseudomonas aeruginosa is a frequently encountered pathogen that is involved in acute and chronic lung infections. Lectin-mediated bacterium-cell recognition and adhesion are critical steps in initiating P. aeruginosa pathogenesis. This study was designed to evaluate the contributions of LecA and LecB to the pathogenesis of P. aeruginosa-mediated acute lung injury. Using an in vitro model with A549 cells and an experimental in vivo murine model of acute lung injury, we compared the parental strain to lecA and lecB mutants. The effects of both LecA- and Lec B-specific lectin-inhibiting carbohydrates (a-methyl-galactoside and a-methyl-fucoside, respectively) were evaluated. In vitro, the parental strain was associated with increased cytotoxicity and adhesion on A549 cells compared to the lecA and lecB mutants. In vivo, the P. aeruginosa-induced increase in alveolar barrier permeability was reduced with both mutants. The bacterial burden and dissemination were decreased for both mutants compared with the parental strain. Coadministration of specific lectin inhibitors markedly reduced lung injury and mortality. Our results demonstrate that there is a relationship between lectins and the pathogenicity of P. aeruginosa
Anglicky
Pseudomonas aeruginosa is a frequently encountered pathogen that is involved in acute and chronic lung infections. Lectin-mediated bacterium-cell recognition and adhesion are critical steps in initiating P. aeruginosa pathogenesis. This study was designed to evaluate the contributions of LecA and LecB to the pathogenesis of P. aeruginosa-mediated acute lung injury. Using an in vitro model with A549 cells and an experimental in vivo murine model of acute lung injury, we compared the parental strain to lecA and lecB mutants. The effects of both LecA- and Lec B-specific lectin-inhibiting carbohydrates (a-methyl-galactoside and a-methyl-fucoside, respectively) were evaluated. In vitro, the parental strain was associated with increased cytotoxicity and adhesion on A549 cells compared to the lecA and lecB mutants. In vivo, the P. aeruginosa-induced increase in alveolar barrier permeability was reduced with both mutants. The bacterial burden and dissemination were decreased for both mutants compared with the parental strain. Coadministration of specific lectin inhibitors markedly reduced lung injury and mortality. Our results demonstrate that there is a relationship between lectins and the pathogenicity of P. aeruginosa
Návaznosti
| GA303/09/1168, projekt VaV |
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| MSM0021622413, záměr |
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