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1.
New Microbes New Infect ; 29: 100510, 2019 May.
Artículo en Inglés | MEDLINE | ID: mdl-30899519

RESUMEN

We report an outbreak Bacillus cereus causing postpartum bacteraemia in the maternity ward and delivery room. Spores transferred by the hands and gloves of the staff in the maternity ward contaminated equipment in these two areas.

2.
Scand J Immunol ; 67(2): 193-203, 2008 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-18086260

RESUMEN

TNF-alpha production has a central role in the development and progression of Pseudomonas aeruginosa septic shock. We have previously shown that P. aeruginosa slime-glycolipoprotein (slime-GLP) is the most potent stimulant compared to P. aeruginosa lipopolysaccharide (LPS), for TNF-alpha production and NF-kB activation in human monocytes. Herein, we show that secretion of TNF-alpha by fresh human monocytes, induced by P. aeruginosa slime-GLP, LPS or viable bacteria, was paralleled by phosphorylation and/or activation of Mitogen-activated Protein Kinases (MAPKs) ERK1/2, p38 as well as c-Jun NH(2)-terminal kinase. TNF-alpha levels were significantly reduced by ERK1/2 inhibitor (PD98059), or p38 inhibitor (SB203580). Combination of both inhibitors almost abolished TNF-alpha induction. Pseudomonas aeruginosa slime-GLP differed from the P. aeruginosa-LPS only regarding the strength of p38 and ERK1/2 activation, with slime-GLP leading to a stronger activation of p38 and ERK1/2. Involvement of TLR2 and TLR4 for phosphorylation of p38 and ERK1/2 was shown using specific blocking anti-TLR2 and anti-TLR4 antibodies. Activation of both p38 and ERK1/2 induced by P. aeruginosa slime-GLP was dramatically reduced in the presence of anti-TLR2 and to a lesser degree in the presence of anti-TLR4, whereas the P. aeruginosa-LPS-induced stimulation was inhibited only in the presence of anti-TLR4. Our data show that P. aeruginosa viable bacteria, through slime-GLP, stimulate specific members of the MAPKs more efficiently than the P. aeruginosa-LPS, involving mainly TLR2.


Asunto(s)
Proteínas Quinasas Activadas por Mitógenos/metabolismo , Monocitos/inmunología , Infecciones por Pseudomonas/inmunología , Pseudomonas aeruginosa/inmunología , Receptor Toll-Like 2/inmunología , Receptor Toll-Like 4/inmunología , Factor de Necrosis Tumoral alfa/biosíntesis , Proteínas Bacterianas/inmunología , Proteínas Bacterianas/farmacología , Western Blotting , Flavonoides/farmacología , Humanos , Imidazoles/farmacología , Lipopolisacáridos/inmunología , Lipopolisacáridos/farmacología , Proteínas Quinasas Activadas por Mitógenos/antagonistas & inhibidores , Monocitos/efectos de los fármacos , Monocitos/enzimología , Fosforilación , Inhibidores de Proteínas Quinasas/farmacología , Piridinas/farmacología , Factor de Necrosis Tumoral alfa/inmunología
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