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Blood, Vol. 92 No. 7 (October 1), 1998:
pp. 2345-2352
Overlapping Functions of E- and P-Selectin in Neutrophil
Recruitment During Acute Inflammation
Jonathon W. Homeister,
Mengkun Zhang,
Paul S. Frenette,
Richard O. Hynes,
Denisa D. Wagner,
John B. Lowe, and
Rory M. Marks
From the Departments of Pathology and Internal Medicine and the
Howard Hughes Medical Institute at The University of Michigan Medical
Center, Ann Arbor, MI; the Center for Cancer Research, the Department
of Biology, and the Howard Hughes Medical Institute, Massachusetts
Institute of Technology, Cambridge, MA; and The Center for Blood
Research, and the Department of Pathology, Harvard Medical School,
Boston, MA.
Selectin adhesion molecules mediate leukocyte rolling on activated
endothelium, a prerequisite to leukocyte accumulation at sites of
inflammation. The precise role of each selectin (E-, P-, and L-) in
this process is unclear and may vary depending on the particular
inflammatory stimulus, vascular bed, leukocyte subset, and species;
most data suggest discrete functional roles for each selectin. To
define the relative roles of E- and P-selectin in mediating neutrophil
accumulation in acute dermal inflammation, mice genetically deficient
in E-selectin, P-selectin, or both E- and P-selectin were injected
intradermally with zymosan. Luminal endothelial expression of E- and
P-selectin in response to zymosan was documented in wild-type mice by
intravenous administration of fluorochrome-labeled anti-E- and
anti-P-selectin antibodies. In mice deficient in E- or P-selectin,
neutrophil accumulation was unchanged or only subtly reduced relative
to wild-type control mice. In mice deficient in both E- and P-selectin,
neutrophil accumulation was significantly reduced (87% at 4 hours and
79% at 8 hours). These data demonstrate that, in this model of acute inflammation, there is considerable overlap in the functions of E- and
P-selectin; loss of both selectins was required to impair neutrophil
accumulation.
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