| First Author | Tang T | Year | 1996 |
| Journal | J Clin Invest | Volume | 97 |
| Issue | 11 | Pages | 2485-90 |
| PubMed ID | 8647940 | Mgi Jnum | J:107411 |
| Mgi Id | MGI:3621099 | Doi | 10.1172/JCI118695 |
| Citation | Tang T, et al. (1996) Cytokine-induced meningitis is dramatically attenuated in mice deficient in endothelial selectins. J Clin Invest 97(11):2485-90 |
| abstractText | Leukocyte accumulation in cerebrospinal fluid and disruption of the blood-brain barrier are central components of meningitis and are associated with a poor prognosis. Genetically engineered deficiencies or functional inhibition of endothelial leukocyte adhesion receptors P-, or P- plus E-selectins, lead to deficits in leukocyte rolling and extravasation. However, their impact on meningeal inflammation has not been tested previously. An acute cytokine-induced meningitis model associated with significant cerebrospinal fluid leukocyte accumulation (averaging 14,000 leukocytes/microl as early as 4 h) and blood-brain barrier permeability was developed in adult mice. This model was applied to mice deficient in P-selectin and mice doubly deficient in P- and E-selectins. Partial inhibition of cerebrospinal fluid leukocyte influx and permeability was noted in P-selectin-deficient mice. Mice doubly deficient in P- and E-selectins displayed a near complete inhibition of these parameters. Our results suggest that P- and E-selectins cooperatively contribute to meningitis and that functional blocking of both endothelial selectins in conjunction with antibiotics may provide a therapeutic approach for treatment of bacterial meningitis. |
