Abstract | INTRODUCTION: Streptococcus (S.) pneumoniae is the most common cause of community-acquired pneumonia. The factor V Leiden (FVL) mutation results in resistance of activated FV to inactivation by activated protein C and thereby in a prothrombotic phenotype. Human heterozygous FVL carriers have been reported to be relatively protected against sepsis-related mortality. We here determined the effect of the FVL mutation on coagulation, inflammation, bacterial outgrowth and outcome in murine pneumococcal pneumonia. METHODS: Wild-type mice and mice heterozygous or homozygous for the FVL mutation were infected intranasally with 2*106 colony forming units of viable S. pneumoniae. Mice were euthanized after 24 or 48 hours or observed in a survival study. In separate experiments mice were treated with ceftriaxone intraperitoneally 24 hours after infection and euthanized after 48 hours or observed in a survival study. RESULTS: CONCLUSIONS:
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Authors | Marcel Schouten, Cornelis van't Veer, Joris J T H Roelofs, Marcel Levi, Tom van der Poll |
Journal | Critical care (London, England)
(Crit Care)
Vol. 14
Issue 4
Pg. R145
( 2010)
ISSN: 1466-609X [Electronic] England |
PMID | 20682036
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anti-Bacterial Agents
- factor V Leiden
- Ceftriaxone
- Factor V
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Topics |
- Activated Protein C Resistance
(complications, genetics)
- Animals
- Anti-Bacterial Agents
(therapeutic use)
- Blood Coagulation Tests
- Ceftriaxone
(therapeutic use)
- Factor V
(genetics, physiology)
- Female
- Homozygote
- Lung
(pathology)
- Male
- Mice
- Pneumonia, Pneumococcal
(complications, drug therapy, genetics, pathology)
- Point Mutation
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