Thrombocytopenia impairs host defense during murine Streptococcus pneumoniae pneumonia

Streptococcus pneumoniae is the most common causative pathogen in community-acquired pneumonia. In patients, thrombocytopenia is correlated with an adverse outcome of pneumonia. Platelets can modulate the host response to infection in several ways, that is, by facilitating clot formation, production...

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Vydáno v:Critical care medicine Ročník 43; číslo 3; s. e75
Hlavní autoři: van den Boogaard, Florry E, Schouten, Marcel, de Stoppelaar, Sacha F, Roelofs, Joris J T H, Brands, Xanthe, Schultz, Marcus J, van't Veer, Cornelis, van der Poll, Tom
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.03.2015
Témata:
Animals
Antithrombin III - metabolism
Cytokines - metabolism
Disease Models, Animal
Mice
Peptide Hydrolases - metabolism
Pneumonia, Pneumococcal - epidemiology
Pneumonia, Pneumococcal - immunology
Pneumonia, Pneumococcal - pathology
Purinergic P2Y Receptor Antagonists - pharmacology
Streptococcus pneumoniae
Thrombocytopenia - epidemiology
Thrombocytopenia - immunology
Thrombocytopenia - pathology
Ticlopidine - analogs & derivatives
Ticlopidine - pharmacology
ISSN:1530-0293, 1530-0293
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Shrnutí:Streptococcus pneumoniae is the most common causative pathogen in community-acquired pneumonia. In patients, thrombocytopenia is correlated with an adverse outcome of pneumonia. Platelets can modulate the host response to infection in several ways, that is, by facilitating clot formation, production of antimicrobial proteins, and interaction with neutrophils. We studied the effect of thrombocytopenia during murine pneumococcal pneumonia. Animal study. University research laboratory. Mice. Pneumonia was induced by intranasal inoculation of S. pneumoniae. Platelets were depleted by anti-mouse thrombocyte serum; controls received nonimmunogenic serum. In separate studies, mice were treated with the platelet P2Y12 receptor inhibitor clopidogrel or placebo. Thrombocytopenic mice (platelet counts < 1% of uninfected controls) showed a reduced survival during pneumococcal pneumonia (27% vs 75% among controls; p = 0.003), which was associated with higher bacterial loads in lungs, spleen, and blood. Thrombocytopenic mice showed enhanced coagulation activation (thrombin-antithrombin complexes) in plasma. Proinflammatory cytokine levels were higher in plasma but not in lungs of thrombocytopenic mice. Although clopidogrel treatment strongly prolonged the bleeding time, it did not impact on bacterial loads during pneumococcal pneumonia. Platelets play a protective role during pneumococcal pneumonia independent of their aggregation.
Bibliografie:ObjectType-Article-1
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ISSN:1530-0293
1530-0293
DOI:10.1097/CCM.0000000000000853