| First Author | Homeister JW | Year | 1998 |
| Journal | Blood | Volume | 92 |
| Issue | 7 | Pages | 2345-52 |
| PubMed ID | 9746773 | Mgi Jnum | J:50212 |
| Mgi Id | MGI:1290033 | Doi | 10.1182/blood.v92.7.2345.2345_2345_2352 |
| Citation | Homeister JW, et al. (1998) Overlapping functions of E- and P-selectin in neutrophil recruitment during acute inflammation. Blood 92(7):2345-52 |
| abstractText | 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. |
