Hyperprolactinemia in male NZB/NZW (B/W) F1 mice: accelerated autoimmune disease with normal circulating testosterone
|Published in||Clinical Immunology and Immunopathology. 1994, vol. 71, no. 3, p. 338-343|
|Abstract||It has been proposed that the immunostimulatory hormone, prolactin, is associated with flares of systemic lupus erythematosus (SLE). In autoimmune female NZB/NZW F1 (B/W) mice with accelerated lupus-like disease, hyperprolactinemia accelerated autoimmunity. The current study explored effects of moderate and severe hyperprolactinemia in male B/W mice, which have late-onset SLE. Autoimmune disease in B/W males was assessed by measurement of anti-DNA antibodies (anti-DNA), gp70-anti-gp70 immune complexes (gp70IC), IgM, IgG, and renal function. Serum testosterone concentrations were assayed serially. All mice were necropsied when moribund. Hyperprolactinemic B/W males were characterized by premature appearance of anti-DNA and gp70IC and elevation of IgM and IgG. Hyperprolactinemia accelerated mortality with vasculitis and renal disease compared to control mice. Serum testosterone concentrations were not suppressed. In male B/W mice, chronic hyperprolactinemia stimulated autoimmune disease activity; the deleterious effects of prolactin were not mediated through suppression of the immunoprotective hormone, testosterone. This observation supports the proposed association between elevated prolactin levels and exacerbations of SLE.|
|Keywords||Animals — Antibodies, Antinuclear/analysis — Autoimmune Diseases/etiology — Blood Urea Nitrogen — Body Weight — Disease Models, Animal — Female — Glycoproteins/blood — Hematocrit — Hyperprolactinemia/ metabolism — Immunoglobulins/blood — Leukocyte Count — Lupus Erythematosus, Systemic/metabolism — Male — Mice — Prolactin/blood — Testosterone/blood|
This document has no fulltext available yet, but you can contact its author by using the form below.
|MCMURRAY, R. et al. Hyperprolactinemia in male NZB/NZW (B/W) F1 mice: accelerated autoimmune disease with normal circulating testosterone. In: Clinical Immunology and Immunopathology, 1994, vol. 71, n° 3, p. 338-343. doi: 10.1006/clin.1994.1095 https://archive-ouverte.unige.ch/unige:10943|