Rheumatoid arthritis and psoriatic arthritis synovial fluids stimulate prolactin production by macrophages

Man Wai Tang, Samuel Garcia, Beatriz Malvar Fernandez, Danielle M. Gerlag, Paul-Peter Tak, Kris A. Reedquist

Research output: Contribution to journalArticleAcademicpeer-review

16 Citations (Scopus)

Abstract

Prolactin (PRL) is a neuroendocrine hormone that can promote inflammation. We examined the synovial tissue and fluid levels of PRL in patients with inflammatory arthritis, PRL expression in differentiated M phi s from patients with arthritis and from healthy donors, and the effects of different stimuli on PRL production by M phi s. PRL levels were measured in paired synovial fluid (SF) and peripheral blood of patients with rheumatoid arthritis (RA, n = 19), psoriatic arthritis (PsA, n = 11), and gout (n = 11). Synovial-tissue PRL mRNA expression was measured by quantitative PCR in patients with RA (n = 25), PsA (n = 11), and gout (n = 12) and in M phi s differentiated in SF of patients with RA, PsA, other subtypes of spondyloarthritis (SpA), and gout. Synovial-tissue PRL mRNA expression correlated significantly with clinical disease parameters in patients with RA and PsA, including erythrocyte sedimentation rate (ESR, r = 0.424; P = 0.049) and disease activity score evaluated in 28 joints (DAS28, r = 0.729; P = 0.017). Synovial-tissue PRL expression was similar in RA, PsA, and gout. PRL mRNA expression was detected in monocyte-derived M phi s from patients with RA and was significantly higher (P 0.01) in M phi s differentiated in pooled SF from patients with RA and PsA compared with SpA or gout. PRL production by M phi differentiation in the SF from patients with RA was not further regulated by stimulation with CD40L, IgG, LPS, or TNF. PRL is produced locally in the synovium of patients with inflammatory arthritis. The production of PRL by M phi s was increased by unknown components of RA and PsA SF, where it could contribute to disease progression
Original languageEnglish
Pages (from-to)897-904
JournalJournal of leukocyte biology
Volume102
Issue number3
Early online date2017
DOIs
Publication statusPublished - 2017

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