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Plasminogen Deficiency Differentially Affects Recruitment of
Inflammatory Cell Populations in Mice
Victoria A. Ploplis,
Esther L. French,
Peter Carmeliet,
Desire Collen, and
Edward F. Plow
From the Joseph J. Jacobs Center for Thrombosis and Vascular Biology,
Department of Molecular Cardiology, Cleveland Clinic Foundation,
Cleveland, Ohio; and Flander's Interuniversity Institute for
Biotechnology, Leuven, Belgium.
It is widely held that the plasminogen (Plg) system plays a role in
inflammation through plasmin-mediated directional cell migration.
However, substantial evidence for its involvement in the inflammatory
response has been obtained from indirect studies and lacks firm
biological confirmation. To directly characterize plasminogen's
involvement in the inflammatory response, we used thioglycollate to
induce a peritoneal inflammatory reaction in Plg(+/+),
Plg(+/ ), and Plg(/) mice. At 6 hours
poststimulation, neutrophil recruitment into the peritoneum was maximal
and similar between Plg(+/+), Plg(+/), and
Plg(/) mice. In contrast, monocyte recruitment was
significantly diminished after 24 hours poststimulation in
Plg(/) mice relative to Plg(+/+) mice.
Lymphocyte recruitment also was blunted. Blood monocyte levels in these
mice indicated that diminished recruitment into the peritoneum was not
the result of a diminished source of cells in the circulation.
Macrophage phagocytic function was similar between Plg(+/+)
and Plg(/) mice. This study establishes a direct
involvement of plasminogen in monocyte recruitment during a
representative inflammatory response.
Blood, Vol. 91 No. 6 (March 15), 1998:
pp. 2005-2009
© 1998 by The American Society of Hematology.
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