Gram-Negative Pneumonia Alters Large-Vein Cell-Adhesion Molecule Profile and Potentiates Experimental Stasis Venous ThrombosisObi A.T.a · Andraska E.a · Kanthi Y.b · Luke C.E.a · Elfline M.a · Madathilparambil S.c · Siahaan T.J.d · Jaffer F.A.e · Wakefield T.W.a · Raghavendran K.c · Henke P.K.a
aConrad Jobst Vascular Research Laboratory, University of Michigan Medical School, bDivision of Cardiovascular Medicine, and cSection of Vascular Surgery, Department of Surgery, University of Michigan, Ann Arbor, Mich., dSchool of Pharmacy, University of Kansas, Kansas City, Kans., and eCardiovascular Research Center, Massachusetts General Hospital, Boston, Mass., USA
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Article / Publication Details
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.
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