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Coagulation factor XII regulates inflammatory responses in human lungs
Rosanna Hess, Lukasz Wujak, Christina Hesse
1Malgorzata Wygrecka, PhD, Department of Biochemistry, Faculty of Medicine,, Universities of Giessen and Marburg Lung Center, Friedrichstrasse 24, 35392 Giessen, Germany, Tel.: +49 641 99 47482, Fax: +49 641 99 47509,
Thrombosis and Haemostasis
|August 18, 2017
Summary
The contact system, including factor XIIa, is activated in acute respiratory distress syndrome (ARDS) lungs, driving inflammation. Inhibiting factor XII may offer a new ARDS therapy.
Area of Science:
- Pulmonary Medicine
- Coagulation Cascade
- Inflammatory Response
Background:
- Acute Respiratory Distress Syndrome (ARDS) involves alveolar hypercoagulation and inflammation.
- The role of the coagulation contact system in ARDS pathogenesis is not fully understood.
Purpose of the Study:
- To investigate contact system activation in ARDS lungs.
- To determine the impact of contact system components on inflammatory mediator release in the lung.
Main Methods:
- Analysis of bronchoalveolar lavage fluid (BALF) from ARDS patients and controls for contact system components.
- Assessment of cytokine and chemokine expression in human precision cut lung slices (PCLS) using PCR arrays.
Main Results:
- Contact system activation, marked by elevated factor XIIa, plasma kallikrein, and bradykinin, was rapid in ARDS lungs.
- Factor XII levels correlated with disease severity and tumor necrosis factor-alpha (TNF-α) levels.
- Factor XII induced pro-inflammatory cytokine and chemokine release in PCLS independently of the kallikrein-kinin pathway.
Conclusions:
- Factor XII accumulation in ARDS lungs contributes to inflammatory mediator release and is linked to clinical outcomes.
- Targeting factor XII may represent a novel therapeutic strategy for ARDS, potentially mitigating inflammation without disrupting essential hemostasis.
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