| First Author | Sun X | Year | 1997 |
| Journal | Am J Physiol | Volume | 273 |
| Issue | 1 Pt 1 | Pages | G56-61 |
| PubMed ID | 9252509 | Mgi Jnum | J:41968 |
| Mgi Id | MGI:894882 | Doi | 10.1152/ajpgi.1997.273.1.G56 |
| Citation | Sun X, et al. (1997) P-selectin-deficient mice are protected from PAF-induced shock, intestinal injury, and lethality. Am J Physiol 273(1 Pt 1):G56-61 |
| abstractText | In a previous study, we showed that anti-CD11b or anti-CD18 antibody markedly attenuated platelet-activating factor (PAF)-induced shock and intestinal necrosis in rats, whereas anti-P-selectin anti-body was ineffective. Here we used genetically altered mice to study the mechanism of PAF in mice. We found that P-selectin-deficient mice are completely protected from the adverse effects of PAF with no mortality or intestinal injury and only mild hemoconcentration and transient hypotension. In contrast, CD18- or intercellular adhesion molecule 1 (ICAM-1)-deficient mice were not protected from PAF-induced tissue injury and death. However, when ICAM-1-, but not CD18-, deficient mice were pretreated with fucoidin, the adverse effects of PAF were markedly reduced; survival was 100%, although hypotension still developed. Neutrophil-depleted mice were protected from PAF-induced intestinal injury but still developed hypotension and hemoconcentration. PAF increases peripheral blood neutrophil counts, probably by inducing granulopoiesis, since neutrophil-depleted mice still showed granulocytosis 60 min after PAF. Thus P-selectin plays an important role in PAF-induced injury in mice, and the selectins and the integrin-ICAM-1 system work in concert to mediate the inflammatory response to PAF in vivo. |
