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Corticosterone Treatment of Pregnant Low Dose Endotoxin‐Treated Rats: Inhibition of the Inflammatory Response
Author(s) -
FAAS M.M.,
SLOT K.,
KOITER T.R.,
SCHUILING G.A.
Publication year - 2000
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.8755-8920.2000.440308.x
Subject(s) - corticosterone , medicine , endocrinology , saline , inflammation , kidney , cholesterol , chemistry , hormone
PROBLEM: Can the endotoxin‐induced inflammatory response, underlying experimental pre‐eclampsia, in pregnant rats be inhibited by corticosterone?
METHOD OF STUDY: On day 10 of pregnancy, rats were implanted with pellets containing 25% corticosterone and 75% cholesterol ( n =10) or with 100% cholesterol‐pellets ( n =10). On day 14 of pregnancy, rats were infused with either endotoxin (1.0 μg/kg bw) or saline. Three days later, they were sacrificed. Cryostat kidney sections were immunohistologically stained for the presence of neutrophils (PMN) and monocytes (M∅) and the expression of inflammation‐associated adhesion molecules.
RESULTS: In cholesterol‐treated rats, endotoxin significantly increased glomerular numbers of PMN and M∅, glomerular expression of ICAM‐1 and VCAM‐1 and glomerular numbers of LFA‐1 and VLA‐4‐positive cells as compared with saline. Corticosterone treatment significantly inhibited glomerular infiltration of PMN, M∅ and LFA‐1 positive cells after endotoxin infusion. It did not affect glomerular ICAM‐1 or VCAM‐1 expression or numbers of VLA‐4 positive cells.
CONCLUSIONS: It is concluded that pre‐treatment with corticosterone inhibits the low dose endotoxin‐induced glomerular inflammatory reaction in pregnant rats, most likely by inhibiting LFA‐1 expression, thereby decreasing the adhesiveness of inflammatory cells for activated endothelial cells.