Original article Prolactin synthesis by lymphocytes from patients with systemic sclerosis Joanna Czuwara-Ladykowska a , Justyna Sicinska a , Malgorzata Olszewska b , Izabela Uhrynowska-Tyszkiewicz b , Lidia Rudnicka a,c, * a Department of Dermatology CSK MSWiA, ul. Woloska 137, 02-507 Warsaw, Poland b Department of Dermatology, Warsaw Medical School, ul. Koszykowa 82a, 02-008 Warsaw, Poland c Polish Academy of Sciences, Palace of Culture and Science, Plac Defilad 1, Skr. Poczt., 00-901 Warsaw, Poland Received 16 January 2006; accepted 7 February 2006 Available online 31 March 2006 Abstract Systemic sclerosis (SSc) is an autoimmune disease characterized by fibrosis of the skin and internal organs. It has been demonstrated that serum prolactin levels are increased in patients with various connective tissue diseases. The aim of this study was to investigate the possible source of excessive prolactin synthesis in SSc and its effects on immune cells. The study group consisted of 52 patients with diffuse SSc (44 women and eight men) and 52 age and sex matched healthy controls. The methods used were: ELISA and indirect immunofluorescence. Our results show significantly elevated level of prolactin in male and female patients with SSc and increased prolactin production by SSc lympho- cytes as compared to healthy donors X lymphocytes (25.4 ± 11.0 vs. 13.4 ± 5.0 absorbance units). Patients X and healthy controls X lympho- cytes, showed equal presence of prolactin receptors. Soluble interleukin 2 receptor (CD25) concentration, was significantly higher in supernatants of prolactin stimulated lymphocytes, as compared to non-stimulated lymphocytes. We conclude that lymphocytes might contribute to elevated prolactin levels in patients with SSc and that these cells themselves may be sensitive to prolactin stimulation. Therefore, a pharmacologic attempt to lower prolactin levels in patients with SSc could proof beneficial. © 2006 Elsevier SAS. All rights reserved. Keywords: Scleroderma; T cells; Interleukin 2 1. Introduction Systemic sclerosis (SSc) is a connective tissue disease char- acterized by microvascular obliteration and increased deposi- tion of collagen in extracellular matrix, resulting in progressive thickening of the skin and fibrosis of various internal organs [1]. Etiology of SSc is unknown but several data indicate that activation of the immune system may be a primary cause for the development of tissue fibrosis [2]. SSc occurs in women of childbearing age at least five times more frequently than in men [3], what may suggest a patho- genic role of hormones in this disease. Accumulating body of evidence suggests that the anterior pituitary hormone prolactin (PRL) might play a pathogenic role in auto-immune connective tissue diseases, including SSc [4–7]. PRL serum levels have been shown to be significantly elevated in female patients with SSc but the source of elevated PRL in SSc has never been determined [4,8,9]. The aim of this study was to evaluate serum levels of pro- lactin in both, women and men with SSc, to determine whether there might be an extrapituitary source of prolactin in SSc pa- tients and to assess whether prolactin might effect the immune system in a manner which could suggest its potential role in deteriorating SSc. 2. Materials and methods The study was performed in 52 SSc patients and 52 age and sex matched healthy volunteers. All SSc patients met the clas- sification criteria established by the American College of Rheumatology [10]. Forty-four patients were females and eight http://france.elsevier.com/direct/BIOPHA/ Biomedicine & Pharmacotherapy 60 (2006) 152–155 Abbreviations: dcSSc, diffuse cutaneous systemic sclerosis; ELISA, enzyme-linked immunosorbent assay; FCS, fetal calf serum; IIF, indirect immunofluorescence; PBMC, peripheral blood mononuclear cells; sIL-2R, soluble receptor of interleukin 2; SSc, systemic sclerosis. * Corresponding author. Tel.: +48 695 303 182, fax: +48 225 081 492. E-mail addresses: czuwaraj@yahoo.com (J. Czuwara-Ladykowska), justyna.sicinska@wp.pl (J. Sicinska), malgorzataolszewska@yahoo.com (M. Olszewska), ityszk@gmail.com (I. Uhrynowska-Tyszkiewicz), lidiarudnicka@yahoo.com (L. Rudnicka). 0753-3322/$ - see front matter © 2006 Elsevier SAS. All rights reserved. doi:10.1016/j.biopha.2006.02.007