TY - JOUR
T1 - A platelet-activating factor antagonist inhibits interleukin 1-induced inflammation
AU - Rubin, Richard M.
AU - Rosenbaum, James T.
N1 - Funding Information:
Supported in part by grants EY 06477 and EY 06484 from the National Eye Institute. Dr. Rubin is a fellow of the Association for Research in Vision and Ophthalmology funded through Alcon Laboratories, Znc. Dr. Rosenbaum is the recipient of a Dolly Green Scholar Award from Research to Prevent Blindness. SRI 63-441 was generously provided by Dean Handley, Ph.D. of the Sandoz Research Institute. Recombinant human interleukin l-alpha was generously provided by Peter Lomedico, Ph.D., Richard Chizzonite, Ph.D., Alvin Stern, Ph.D. and Swapan Roy, Ph.D. of Hoffman LaRoche, Inc. We also wish to thank Steven Hefeneider, Ph.D. of the Portland Veterans Administration Medical Center assaying interleukin 1 activity.
PY - 1988/7/15
Y1 - 1988/7/15
N2 - Treatment with a platelet-activating factor receptor antagonist, SRI 63-441, inhibited interleukin 1-induced increases in vascular permeability and leukocyte infiltration in the rabbit eye following the intravitreal injection of human interleukin 1-alpha. Treatment with the prostaglandinsynthetase inhibitor, flurbiprofen, or the corticosteroid, prednisolone, resulted in comparable attenuation of the increase in vascular permeability. In contrast to the effect of flurbiprofen, SRI 63-441 did not reduce interleukin 1-induced increases in prostaglandin E2 levels. Combined treatment with the platelet-activating factor antagonist and inhibitors of prostaglandin synthesis nearly prevented interleukin 1-induced increases in vascular permeability or cellular infiltration. These findings suggest a role for platelet-activating factor in interleukin 1-induced inflammation. Platelet-activating factor and prostaglandins may act synergistically as mediators of interleukin 1-induced vascular permeability.
AB - Treatment with a platelet-activating factor receptor antagonist, SRI 63-441, inhibited interleukin 1-induced increases in vascular permeability and leukocyte infiltration in the rabbit eye following the intravitreal injection of human interleukin 1-alpha. Treatment with the prostaglandinsynthetase inhibitor, flurbiprofen, or the corticosteroid, prednisolone, resulted in comparable attenuation of the increase in vascular permeability. In contrast to the effect of flurbiprofen, SRI 63-441 did not reduce interleukin 1-induced increases in prostaglandin E2 levels. Combined treatment with the platelet-activating factor antagonist and inhibitors of prostaglandin synthesis nearly prevented interleukin 1-induced increases in vascular permeability or cellular infiltration. These findings suggest a role for platelet-activating factor in interleukin 1-induced inflammation. Platelet-activating factor and prostaglandins may act synergistically as mediators of interleukin 1-induced vascular permeability.
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U2 - 10.1016/0006-291X(88)90704-8
DO - 10.1016/0006-291X(88)90704-8
M3 - Article
C2 - 3260779
AN - SCOPUS:0023711475
SN - 0006-291X
VL - 154
SP - 429
EP - 436
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -