beta-endorphin and Proteinuria

Complex interactions between the neuroendocrine and the immune systems are present in autoimmune diseases. The central opioid peptide beta-endorphin (BE) has been shown to modulate peripheral immune responses in normal animals. In the present study we analyze the hypothalamic concentrations of this peptide in two models of spontaneous autoimmune disease, the MRL [corrected] lpr/lpr mouse, that develops a lupus-like autoimmune disease, and the obese strain (OS) chickens afflicted with spontaneous autoimmune thyroiditis. In both instances, hypothalamic concentrations of BE are significantly lower than normal controls. In MRL [corrected] lpr/lpr mice, BE is already lower at 1 month of age, when no clinical sign of the disease is yet present. Similarly, low levels of BE are observed in OS chickens before the onset of thyroiditis, i.e., already at the embryonic stage. Moreover, a further decrease of BE is observed in OS chickens in correspondence with the first signs of thyroid mononuclear infiltration. Considering the immunosuppressive effects exerted by central BE, these results are suggestive of the fact that in autoimmune disease prone animals the low hypothalamic concentrations may be one of several factors predisposing for the development of autoimmune disease.

Topics: Animals; Autoimmune Diseases; beta-Endorphin; Chickens; Female; Hypothalamus; Male; Mice; Mice, Inbred MRL lpr; Neuroimmunomodulation; Obesity; Proteinuria; Substance P; Thyroiditis, Autoimmune

1. Radioimmunoassay of the opiate, beta-endorphin, in mouse sera, indirect measurement of estrogen by examination of vaginal smears and indirect measurement of androgens by electrophoresis of major urinary proteins (MUP) revealed that beta-endorphin increases while estrogen and androgen levels decrease in mice with chronic Schistosoma mansoni infection. 2. Injections of the opiate antagonist, naltrexone, reversed the effects of schistosomiasis on estrogen and androgen levels. 3. Because opiates are known to inhibit the secretion of releasing hormones by the hypothalamus, the data suggest that the inhibition of hypothalamic-pituitary-gonadal function that occurs in chronically infected male and female mice results from excessive beta-endorphin. 4. It is also suggested that the excessive beta-endorphin may be secreted by T-lymphocytes and possibly macrophages involved in the cell-mediated immune response (CMIR) to the ova.

Topics: Androgens; Animals; beta-Endorphin; Estrogens; Estrus; Female; Mice; Mice, Inbred C57BL; Naltrexone; Proteinuria; Schistosomiasis mansoni