title: Increased levels of prolactin during, but not after, the immunisation with rat collagen II enhances the course of arthritis in DBA/1 mice.
abstract: In addition to its well known effects on reproductive organs and lactation the pituitary hormone prolactin (PRL) also influences immune functions. The present investigation was performed in order to clarify the regulatory role of prolactin in autoimmune disease by using the collagen II arthritis model. Groups of virgin female DBA/1 mice were subjected to different short-term treatment protocols (5-10 days) with rat PRL and the drugs bromocriptine (inhibits prolactin secretion) and haloperidol (enhances prolactin secretion). Treatments were performed at different stages of disease development, and effects on clinical scores, anti-collagen II antibody titres as well as agalactosyl IgG levels were recorded. The effects of the treatment protocols on serum PRL levels were assessed by using a radioimmunoassay (RIA) system. Although the accumulated results of the present study indicate that PRL does not fulfil a major role in the regulation of collagen II arthritis, some interesting observations were made. High levels of PRL (PRL injections) made the arthritis worse only if treatment was performed during the induction stage of the disease. Bromocriptine treatment during the immunisation period did not significantly affect the course of arthritis, but treatment at later stages tended to cause exacerbation (significant at the onset period only). These results indicate that PRL has different effects during early and late stages of the development of collagen II-induced arthritis.
authors.affiliation: Department of Molecular Physiology, AFRC Institute of Animal Physiology and Genetics Research, Bab'aham, Cambridge, U.K.
authors.forename: R
authors.initials: R
authors.lastname: Mattsson
authors.forename: A
authors.initials: A
authors.lastname: Mattsson
authors.forename: I
authors.initials: I
authors.lastname: Hansson
authors.forename: R
authors.initials: R
authors.lastname: Holmdahl
authors.forename: G A
authors.initials: GA
authors.lastname: Rook
authors.forename: A
authors.initials: A
authors.lastname: Whyte
mesh_terms: D000818:Animals; D001168:Arthritis / Q000097:blood* / Q000139:chemically induced / Q000276:immunology; D001971:Bromocriptine / Q000494:pharmacology; D003094:Collagen / Q000276:immunology / Q000633:toxicity*; D005260:Female; D006220:Haloperidol / Q000494:pharmacology; D007114:Immunization; D051379:Mice; D008811:Mice, Inbred DBA; D011388:Prolactin / Q000097:blood*; D051381:Rats; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D001971:Bromocriptine; D011388:Prolactin; D003094:Collagen; D006220:Haloperidol