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Updated: Mar 13, 2026

Stenosis of the Inferior Vena Cava: A Murine Model of Deep Vein Thrombosis
Published on: December 22, 2017
Gram-Negative Pneumonia Alters Large-Vein Cell-Adhesion Molecule Profile and Potentiates Experimental Stasis Venous
Andrea T Obi1, Elizabeth Andraska, Yogendra Kanthi
1Conrad Jobst Vascular Research Laboratory, University of Michigan Medical School, Ann Arbor, Mich., USA.
Background/Aims:
Pneumonia is a significant risk factor for the development of venous thrombosis (VT). Cell-adhesion molecules (CAMs) are linked to the pathogenesis of both pneumonia and VT. We hypothesized that remote infection would confer a prothrombogenic milieu via systemic elevation of CAMs.
Methods:
Lung injury was induced in wild-type (C57BL/6) mice by lung contusion or intratracheal inoculation with Klebsiella pneumoniae or saline controls. K. pneumoniae-treated mice and controls additionally underwent inferior vena cava (IVC) ligation to generate VT.
Results:
Lung-contusion mice demonstrated no increase in E-selectin or P-selectin whereas mice infected with K. pneumoniae demonstrated increased circulating P-selectin, ICAM-1, VCAM-1 and thrombin-antithrombin (TAT) complexes. Mice with pneumonia formed VT 3 times larger than controls, demonstrated significantly more upregulation of vein-wall and systemic CAMs, and formed erythrocyte-rich thrombi.
Conclusion:
Elevated CAM expression was identified in mice with pneumonia, but not lung contusion, indicating that the type of inflammatory stimulus and the presence of infection drive the vein-wall response. Elevation of CAMs was associated with amplified VT and may represent an alternate mechanism by which to target the prevention of VT.
Insights
Pneumonia, unlike lung contusion, elevates cell-adhesion molecules (CAMs) and increases venous thrombosis (VT) risk. This suggests CAMs are a potential target for preventing VT associated with infection.
Area of Science:
- Immunology
- Hematology
- Pulmonary Medicine
Background:
- Pneumonia is a significant risk factor for venous thrombosis (VT).
- Cell-adhesion molecules (CAMs) are implicated in the pathogenesis of both pneumonia and VT.
- Remote infections may create a prothrombotic state through systemic CAM elevation.
Purpose of the Study:
- To investigate the role of cell-adhesion molecules (CAMs) in the development of venous thrombosis (VT) following pneumonia.
- To determine if lung contusion or bacterial pneumonia induces systemic CAM elevation and prothrombotic changes.
Main Methods:
- Induced lung injury in mice via lung contusion or Klebsiella pneumoniae inoculation.
- Assessed circulating CAMs (P-selectin, ICAM-1, VCAM-1) and thrombin-antithrombin complexes.
- Induced VT via inferior vena cava ligation in infected and control mice.
Main Results:
- K. pneumoniae infection, not lung contusion, significantly increased circulating CAMs and thrombin-antithrombin complexes.
- Pneumonia led to 3x larger VT formation compared to controls.
- Increased vein-wall and systemic CAMs were observed in pneumonia-induced VT, with erythrocyte-rich thrombi.
Conclusions:
- Elevated CAM expression is linked to pneumonia-induced VT, but not solely lung contusion.
- The type of inflammatory stimulus and presence of infection drive the vein-wall response.
- CAM elevation presents a potential therapeutic target for preventing infection-associated VT.
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