Monocyte activation, but not granulocyte activation, is inhibited in the presence of developing ovarian follicles.
This study was set up to evaluate the influence of ovarian factors on the acute phase of the endotoxin-induced glomerular inflammatory reaction. Six groups of rats with permanent jugular vein cannulas were used. This included three groups with increased progesterone and/or 17beta-oestradiol concentrations (day 14 pregnant rats, pseudopregnant rats and lactating rats), one group with the presence of developing ovarian follicles (cyclic rats), and two groups with both increased sex hormone concentrations and the presence of developing ovarian follicles (day 14 pregnant rats treated with FSH and day 21 pregnant rats). Rats were infused for 1h with either saline or endotoxin (1 microg/kg body weight) and sacrificed 4h after the infusion. Kidney sections were snap-frozen and prepared for immunohistochemistry. Endotoxin-induced glomerular granulocyte infiltration was increased only in the groups of rats with increased progesterone and/or 17beta-oestradiol concentrations. This could be due to endotoxin-induced ICAM-1 and/or VCAM-1 expression, which was observed in all endotoxin-treated groups and in all endotoxin-treated groups with increased sex hormone concentrations, respectively. It could also be due to an effect on granulocytes per se, since the number of endotoxin-induced CD11b-positive cells in the glomeruli was increased only in the groups with increased sex hormone concentrations. Endotoxin-induced glomerular monocyte infiltration, however, was seen only in those groups in which developing ovarian follicles were lacking (i.e. day 14 pregnant, pseudopregnant and lactating rats), suggesting that developing ovarian follicles produce anti-inflammatory factors. These factors did not have an effect on endothelial or leukocyte adhesion molecule expression. We hypothesize that the presence of elevated progesterone concentrations increased the endotoxin-induced glomerular granulocyte infiltration, while endotoxin-induced glomerular monocyte infiltration was inhibited in the presence of developing ovarian follicles.
Faas
M M
MM
Transplantation Biology and Immunoendocrinology, Department of Pathology and Laboratory Medicine, University Medical Centre Groningen, University of Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. m.m.faas@med.umcg.nl
Moes
H
H
van der Schaaf
G
G
Heineman
M J
MJ
de Vos
P
P
D000210:Acute-Phase Reaction; D000818:Animals; D040881:CD11a Antigen / Q000096:biosynthesis / Q000276:immunology; D039481:CD11b Antigen / Q000096:biosynthesis / Q000276:immunology; D002450:Cell Communication / Q000276:immunology*; D004958:Estradiol / Q000378:metabolism; D005260:Female; D006098:Granulocytes / Q000276:immunology*; D039041:Integrin alpha4beta1 / Q000096:biosynthesis / Q000276:immunology; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis / Q000276:immunology; D007678:Kidney Glomerulus / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D009000:Monocytes / Q000276:immunology*; D006080:Ovarian Follicle / Q000276:immunology*; D011247:Pregnancy; D011374:Progesterone / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis / Q000276:immunology
D040881:CD11a Antigen; D039481:CD11b Antigen; D039041:Integrin alpha4beta1; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D011374:Progesterone; D004958:Estradiol