Coagulation and inflammation

Lipinski, Simone; Bremer, Lars; Lammers, T; Thieme, Florian; Schreiber, S.; Rosenstiel, Philip

doi:10.5482/ha-1134

Cited by 54 publications

(25 citation statements)

References 101 publications

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“…The combination of GSR with the dorsal skinfold chamber model allows the assessment of microcirculatory dysfunction and microvascular thrombosis as key events driving the progression of endotoxin-induced critical illness (36, 37). In line with several studies showing the alteration of the microcirculation upon LPS exposure (38, 39), mice undergoing GSR show the reduced microhemodynamics, thrombocytopenia and leukocytopenia, and the triggering of coagulation and inflammatory responses that can be seen in septic patients (40, 41). Gene-targeted PZ- and ZPI-deficient mice provide a powerful tool to study the specific roles of PZ and ZPI in this scenario (42, 43).…”

Section: Discussionsupporting

confidence: 80%

Contribution of Protein Z and Protein Z-Dependent Protease Inhibitor in Generalized Shwartzman Reaction

Butschkau

Nagel²,

Grambow³

et al. 2013

Critical Care Medicine

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Objective Sepsis, a leading cause of mortality in critically ill patients, is closely linked to the excessive activation of coagulation and inflammation. Protein Z (PZ), a cofactor for the protein Z-dependent protease inhibitor (ZPI), enhances the inhibition of coagulation factor Xa and ZPI inhibits factor XIa in a PZ-independent fashion. The functions of PZ and ZPI in the inflammatory and coagulant responses to septic illness have not been evaluated. Design For induction of generalized Shwartzman reaction (GSR), dorsal skinfold chamber-equipped mice were challenged twice with lipopolysaccharide (0.05 mg/kg bw on day −1 and 5 mg/kg bw 24 h later). Time-matched control animals received equal volumes of saline. Setting University research laboratory. Subjects, Interventions and Measurements Using intravital fluorescence microscopy in ZPI-deficient (ZPI−/−) and PZ-deficient (PZ−/−) mice as well as their wild-type littermates (ZPI+/+, PZ+/+), kinetics of light/dye-induced thrombus formation and microhemodynamics were assessed in randomly chosen venules. Plasma concentrations of CXCL1, IL-6 and IL-10 were measured. Liver and lung were harvested for quantitative analysis of leukocytic tissue infiltration and thrombus formation. Main Results After induction of GSR, all mice showed significant impairment of microhemodynamics, including blood flow velocity, volumetric blood flow and functional capillary density as well as leukocytopenia and thrombocytopenia. Thrombus formation time was markedly prolonged after induction of GSR in all mice, except of ZPI−/− mice, which also had a significantly higher fraction of occluded vessels in liver sections. PZ−/− mice developed the highest concentrations of IL-6 and IL-10 in response to GSR and showed greater leukocytic tissue infiltration than their wild-type littermates. Conclusions In this murine model of GSR, ZPI deficiency enhanced the thrombotic response to vascular injury, whereas PZ deficiency increased inflammatory response.

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Section: Discussionsupporting

confidence: 80%

Contribution of Protein Z and Protein Z-Dependent Protease Inhibitor in Generalized Shwartzman Reaction

Butschkau

Nagel²,

Grambow³

et al. 2013

Critical Care Medicine

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“…In chronic inflammatory diseases however, anti-inflammatory treatment has become clinical routine. For example, inhibition of IL-6 by the first anti-IL-6 antibody, tocilizumab, has been shown to completely block TF-dependent thrombin generation in experimental endotoxemia [23, 96], and tocilizumab will be of special future interest as it has been approved for rheumatoid arthritis.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms by which the coagulation system is altered by inflammatory interactions comprise enhanced synthesis and activation of coagulant proteins, decreased synthesis of anticoagulants, and suppression of fibrinolysis [23]. However, not only inflammation activates coagulation but coagulation in turn perpetuates inflammatory response [24].…”

Section: Introductionmentioning

confidence: 99%

The Interface between Inflammation and Coagulation in Cardiovascular Disease

Demetz

Ott

2012

International Journal of Inflammation

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The intimate connection between coagulation and inflammation in the pathogenesis of vascular disease has moved more and more into focus of clinical research. This paper focuses on the essential components of this interplay in the settings of cardiovascular disease and acute coronary syndrome. Tissue factor, the main initiator of the extrinsic coagulation pathway, plays a central role via causing a proinflammatory response through activation of coagulation factors and thereby initiating coagulation and downstream cellular signalling pathways. Regarding activated clotting factors II, X, and VII, protease-activated receptors provide the molecular link between coagulation and inflammation. Hereby, PAR-1 displays deleterious as well as beneficial properties. Unravelling these interrelations may help developing new strategies to ameliorate the detrimental reciprocal aggravation of inflammation and coagulation.

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“…Another mechanism that seems involved in IUGR development is the inflammatory response, which interestingly has been linked to the coagulation process state [30,31]. Normal pregnancy is associated with increased maternal plasma complement components concentration.…”

Section: Immune Mechanisms and Iugrmentioning

confidence: 99%

Changes in amniotic fluid and umbilical cord serum proteomic profiles of foetuses with intrauterine growth retardation

et al. 2011

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Foetal growth is a result of a complex net of processes, requiring coordination within the maternal, placental, and foetal compartments, the imbalance or lack of which may lead to intrauterine growth restriction (IUGR). IUGR is the major cause of perinatal morbidity and mortality, and is also related to enhanced morbidity and metabolic abnormalities later in life. In the present study, the protein profiles of umbilical cord serum (UCS) and amniotic fluid (AF) of ten IUGR and ten appropriate for gestational age newborns have been analysed by 2-DE, and nanoHPLC-Chip/MS technology. A total of 18 and 13 spots were found to be differentially expressed (p<0.01) in UCS and AF respectively. The unique differentially expressed proteins identified by MS/MS analysis were 14 in UCS, and 11 in AF samples. Protein gene ontology classification indicate that 21% of proteins are involved in inflammatory response, 20% in immune response, while a smaller proportion are related to transport, blood pressure, and coagulation. These results support the conclusion that the IUGR condition alters the expression of proteins involved in the coagulation process, immune mechanisms, blood pressure and iron and copper homeostasis control, offering a new insight into IUGR pathogenesis.

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Coagulation and inflammation

Cited by 54 publications

References 101 publications

Contribution of Protein Z and Protein Z-Dependent Protease Inhibitor in Generalized Shwartzman Reaction

Contribution of Protein Z and Protein Z-Dependent Protease Inhibitor in Generalized Shwartzman Reaction

The Interface between Inflammation and Coagulation in Cardiovascular Disease

Changes in amniotic fluid and umbilical cord serum proteomic profiles of foetuses with intrauterine growth retardation

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