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SummaryBi-directional relationships operate between the hypothalamic-pituitary-gonadal axis and the immune system. Cytokines, peptide hormones and their shared receptors/ligands are used as a common biological language for communication within and between the immune and neuroendocrine systems. Such communication suggests an immunoregulatory role for the brain and a sensory function for the immune system. We used a radioimmunoassay to measure the concentrations of steroid hormones (cortisol, testosterone, estradiol and progesterone) and pituitary hormones [follicle stimulating hormone (FSH), luteinizing hormone (LH) human chorionic gonadotropin (HCG) and prolactin] in peripheral blood plasma from 78 young Gabonese women with chronic filarial infections. We used an enzyme-linked immunosorbent assay to determine the concentrations of four proinflammatory cytokines [tumor necrosis factor-alpha (TNF-a), gamma interferon (IFN-c), interleukin-1 (IL-1) and IL-6] in the same plasma samples. Progesterone was unchanged and all other steroid hormone plasma concentrations were lower in microfilaremic women than in amicrofilaremic women. The concentration of LH was higher in amicrofilaremic women, whereas the prolactin concentration was higher in microfilaremics. The plasma concentrations of TNF-a, IFN-c, IL-1 and IL-6 were higher in microfilaremic women. A strong negative correlation was found between the steroid and pituitary hormones and the pro-inflammatory cytokines. Conversely, a strong positive correlation was found between prolactin and the same cytokines. These data provide first evidence of immune system and hormonal system disturbance during chronic filarial infections and suggest that the observed imbalance should be taken into account in the diagnosis and treatment of filarial infections.

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Background: Immunor (IM28), an analog of dehydroepiandrosterone (DHEA), inhibits human immunodeficiency virus type-1 (HIV-1) by inhibiting reverse transcriptase. We assessed the ability of IM28 to inhibit the cell-cell fusion mediated by HIV envelope glycoprotein in an in vitro system. For this purpose, we co-cultured TF228.1.16, a T-cell line expressing stably HIV-1 glycoprotein envelopes, with an equal number of 293/CD4+, another T cell line expressing CD4, and with the SupT1 cell line with or without IM28.

SUMMARY A thermostable urinary homologue of the plasma aldosterone-binding globulin (ABG), designated ABG-TsU, was isolated and purified by differential ultrafiltratlon, ion exchange chromatography, and gel filtration to electrophoretic homogeneity. Scatchard plot analysis using highly purified ABG-TsU demonstrated reversible high-affinity low-capacity binding at separate sites for aldosterone and dehydroepiandrosterone sulfate (DHEA-SO 4 ). ABG-TsU injected intraperitoneally (i.p.) in male rats resulted in sustained hypertension after 5 to 8 days, characterized after 12 days by no changes in plasma Na + K + , aldosterone, or plasma renin activity (PRA). No histological changes could be detected in the kidneys, brains, or hearts, nor evidence of adrenocortical hyperplasia. This hypertension appears to be aldosterone-dependent since it is prevented by bilateral adrenalectomy or administration of a spironolactone, but not by adrenalectomy when aldosterone is given concomitantly with ABG-TsU. Hemodynamic characterization of this hypertension was carried out in rats after treatment with ABG-TsU or saline i.p. for 14 days. Cardiac output (CO) was measured using the reference sample microsphere method. ABG-TsU-treated rats had significantly higher mean arterial pressure (MAP), systolic blood pressure (SBP), diastolic blood pressure (DBP), and CO, while no difference in total peripheral resistance (TPR) was detected. This new animal model of borderline essential hypertension (EH) induced by ABG-TsU, which has a reversible high-affinity binding for aldosterone, results in adrenal-dependent hypertension due at this early phase to an increase in CO without any change in TPR, which remains inappropriately normal. Increased plasma levels of aldosterone in subjects with EH were found to be linked to a decrease in the metabolic clearance rate (MCR) of aldosterone in the face of a normal or decreased secretion rate.1 The decrease in the MCR of aldosterone wasFrom the