Potential Role of Prolactin in Modulating the Immuno-Inflammatory Response Induced in a Male Rat Model of Rheumatoid Arthritis,MAGDA M. AL HAMZAWI, HANY ELSBAI, LAILA A. ELSAYED and ASMAA M.S. ABD ELWAHAB
Abstract
The role of leukocyte-derived PRL as an autocrine or paracrine factor which regulates cytokines production is supported by previous observations. Thus, PRL can influence the immune system directly through up-regulation of its receptors on inflammatory cells.
Objective: Investigating the effect at different prolactin levels and the gene expression of its receptors in modulating the immuno-inflammatory response in a rat model of collagen induced arthritis (CIA), which was induced by a single dose of bovine collagen type II emulsified in complete Freund's adjuvant injected at the base of each rat's tail.
Material and Methods: 60 adults normal male ratswere divided into Group (1): Normal control group (n=10) vehicle-treated rats. Group (II) CIA group (n=50) ratswere randomly subdivided into the following: GroupIIA: Untreated group of CIA rats, group (IIB) CIA rats treated with metoclopramide, group (IIC): CIA rats treated with bromocriptine (BCT), group (IID): CIA rats treated with prednisone intake and group (IIE): CIA rats treated with a combination of bromocriptine and prednisone. The parameters estimated in the studied groups were plasma levels of TNF-a, IgG and RF the total and differential lymphocytic counts, monocytic count. Also the levels of synovial TNF-a and PRL-R gene expression on peripheral leucocytes and tissue homogenate were evaluated. To further assess the contribution of prolactin on immune response, the plasma and supernatant PRL levels were mea-sured.
Results: A positive strong correlation between PRL levels and arthritic index in CIA animals was clearly apparent when the experimental rats were treated with metoclopramide. On the other hand, when CIA rats were given bromocryptine, clinical and histopathological improvement were observed.
Conclusion: PRL hypersecretion shifts the balance in the immune response towards higher activity of the immune system cells, which indicated the contribution of PRL to the exacerbation of the disease events.