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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Prolactin in murine systemic lupus erythematosus
1GV (Sonny) Montgomery VA Hospital and the Division of Rheumatology and Molecular Immunology, Department of Medicine, University of Mississippi Medical Center, Jackson 39216, USA. Robert.McMurray@med.va.gov
Lupus
|November 28, 2001
Summary
Elevated prolactin levels worsen autoimmune diseases like lupus in mice. Lowering prolactin with bromocriptine may be a potential therapy for systemic lupus erythematosus (SLE) patients.
Area of Science:
- Immunology
- Endocrinology
- Autoimmune Diseases
Background:
- Murine systemic lupus erythematosus (SLE) shares key autoimmune features with human SLE.
- Elevated serum prolactin (hyperprolactinemia) is implicated in the development and progression of murine lupus.
- Hormonal influences, including estrogen and androgens, modulate autoimmune responses in SLE models.
Purpose of the Study:
- To investigate the role of prolactin in the pathogenesis of murine SLE.
- To evaluate the therapeutic potential of suppressing prolactin in autoimmune disease models.
- To understand the interplay between prolactin and other sex hormones in immune modulation.
Main Methods:
- Utilizing murine models of systemic lupus erythematosus (SLE).
- Administering bromocriptine to suppress serum prolactin concentrations.
- Observing the effects of prolactin modulation on autoimmune disease progression.
Main Results:
- Hyperprolactinemia was found to stimulate the appearance or progression of murine lupus.
- Estrogen potentiated the autoimmune acceleration by prolactin.
- Bromocriptine-induced suppression of prolactin inhibited the development of murine SLE.
- These effects were independent of the immunosuppressive actions of androgens.
Conclusions:
- Prolactin acts as an immunostimulatory agent in autoimmune diseases such as SLE.
- Therapeutic strategies aimed at lowering serum prolactin concentrations may benefit SLE patients.
- Further research in murine SLE models is crucial for understanding hormonal immunomodulation and developing novel therapies.
