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Short Communications |
-/- and MCP-1-/- Mice
****
From the Department of Microbiology and Immunology,*
Burn and Shock Trauma Institute,
the
Departments of Surgery
and Cell
Biology, Neurobiology, and Anatomy,
Immunology
and Aging Program,**
Loyola University Medical Center,
Maywood, Illinois; the Department of Immunology,¶
Schering-Plough Research Institute, Kenilworth, New Jersey; and the
Department of Adult Oncology,||
Dana-Farber Cancer
Institute, Boston, Massachusetts
A salient feature of normal wound healing is the development and
resolution of an acute inflammatory response. Although much is known
about the function of inflammatory cells within wounds, little
is known about the chemotactic and activation signals that influence
this response. As the CC chemokines macrophage inflammatory
protein-1
(MIP-1) and monocyte chemotactic protein-1 (MCP-1) are
abundant in acute wounds, wound repair was examined in
MIP-1-/- and MCP-1-/- mice.
Surprisingly, wound re-epithelialization,
angiogenesis, and collagen synthesis in
MIP-1-/- mice was nearly identical to wild-type
controls. In contrast, MCP-1-/- mice displayed
significantly delayed wound re-epithelialization, with the
greatest delay at day 3 after injury (28 ± 5%
versus 79 ± 14% re-epithelialization,
P < 0.005). Wound angiogenesis was also delayed in
MCP-1-/- mice, with a 48% reduction in capillary
density at day 5 after injury. Collagen synthesis was impeded as
well, with the wounds of MCP-1-/- mice containing
significantly less hydroxyproline than those of control mice (25
± 3 versus 50 ± 8 µg/wound at day 5,
P < 0.0001). No change in the number of wound
macrophages was observed in MCP-1-/- mice,
suggesting that monocyte recruitment into wounds is independent of this
chemokine. The data suggest that MCP-1 plays a critical role in healing
wounds, most likely by influencing the effector state of
macrophages and other cell types.
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