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ABSTRACT

The function of blood and uterine luminal neutrophils from ovariectomized mares treated with ovarian steroids was investigated 18 h after intrauterine infusion of 1 × 10⁹ Streptococcus zooepidemicus. Random migration of blood neutrophils under agarose was reduced by treatment with progesterone compared with that of neutrophils from oestradiol-treated and control mares. In-vitro addition of progesterone to blood neutrophils from acyclic ponies also reduced migration. Uterine neutrophils did not migrate under agarose which was probably an effect of bacterial phagocytosis. Hormone treatment had little effect on phagocytosis of yeast blastospores by blood neutrophils. Phagocytosis by uterine neutrophils from oestradiol-treated and control mares was significantly better than that by blood neutrophils. In progesterone-treated mares, however, phagocytosis by uterine neutrophils was significantly lower than that in the other two treatment groups and was similar to that measured in blood neutrophils.

The results indicate a marked effect of progesterone in reducing both migration of blood neutrophils and phagocytosis by uterine neutrophils.

J. Endocr. (1987) 112, 443–448

Abstract

Treatment of rats with human chorionic gonadotrophin (hCG) induced in the testes an inflammation-like reaction characterized by migration of leukocytes into the interstitial space. In order to find out whether hCG acts in a direct manner in this process, we tested peripheral human blood leukocyte attraction by hCG in vitro. Chemotaxis through cellulose nitrate to gradients of test substances was measured using a 48-well microchemotaxis chamber. Human CG was found to be a potent attractor of neutrophils, monocytes and lymphocytes in vitro in the picomolar concentration range. Checkerboard analyses revealed that the type of migration depends on positive concentration gradients of hCG. The chemoattractant nature of hCG is consistent with its having a role to play in regulation of tissue accumulation of these cells within the reproductive tract.

Journal of Endocrinology (1994) 142, 167–170

ABSTRACT

The biological potencies of recombinant human insulin-like growth factor-I (IGF-I) and two of its analogues were examined for hydrogen peroxide release by neutrophils and blastogenesis by mononuclear cells. The binding affinities of these peptides for bovine serum IGF-binding proteins (IGFBPs) and IGF-I receptors on bovine neutrophils and mononuclear cells were also investigated. Relative to control treatment containing no IGF-I, preincubation of neutrophils with 12·5 μg/l of IGF-I, des(1–3)IGF-I (an analogue of human IGF-I lacking the N-terminal tripeptide Gly-Pro-Glu) and long R³ IGF-I (an analogue of human IGF-I with arginine replacing glutamate at position 3 of human IGF-I and the N-terminal extension Met-Phe-Pro-Ala-Met-ProLeu-Ser-Ser-Leu-Phe-Val-Asn) increased the release of H₂O₂ by 65%, 64% and 32% respectively. However, the difference in stimulating the release of H₂O₂ between long R³ IGF-I and other two (IGF-I and des(1–3)IGF-I) was reduced at a dosage of 100 μg/l. In the absence or presence of 2·5% fetal calf serum (FCS), 100 μg/l of IGF-I, des(1–3)IGF-I but not long R³ IGF-I significantly stimulated thymidine incorporation into mononuclear cells. In addition, des(1–3)IGF-I was more potent than IGF-I in stimulating thymidine incorporation into mononuclear cells in the presence of 2·5% FCS. IGF-I displaced ¹²⁵I-labelled IGF-I binding to serum IGFBPs with half-maximal inhibitory concentrations of approximately 1·5 nmol/1, while des(1–3)IGF-I and long R³ IGF-I only inhibited binding by 20% and 6% respectively, even at a concentration of 35 nmol/l. Similar affinities for IGF-I receptors on neutrophils and mononuclear cells were shown for IGF-I and des(1–3)IGF-I. Conversely, much lower affinities for these receptors were demonstrated for long R³ IGF-I. These results suggest that the biological activities of IGF-I and its analogues in cells of the bovine immune system depend on their binding characteristics both to receptors and to binding proteins.

Journal of Endocrinology (1993) 139, 259–265