Background/Purpose: Prolactin (PRL), the hormone essential for lactation, may protect against joint damage in rheumatoid arthritis. PRL frequently increases in the circulation of patients with rheumatoid arthritis, and eliciting hyperprolactinemia in rats before or after inducing the adjuvant model of inflammatory arthritis reduced chondrocyte apoptosis, proinflammatory cytokine expression, pannus formation, joint swelling, and pain (Adan et al., J Clin Invest 123:3902, 2013). 

Methods: To better understand the role of PRL in inflammatory arthritides, antigen-induced arthritis (AIA) was induced in PRL receptor-deficient (Prlr^-/-) mice from two susceptible genetic backgrounds (C57BL/6 and 129Svj). On day 0, preimmunized or control animals were injected into the knee joint with methylated-BSA antigen (mBSA) or vehicle, respectively, and parameters of inflammation were evaluated at days -1, +1, +3, and +5 post-mBSA. 

Results: In the 129Svj strain, Prlr^-/- mice showed an earlier onset of AIA but similar clinical severity (joint swelling and pain) compared to wild type mice. However, PRLR-deficient mice had a two-fold increase in synovial hyperplasia and higher levels of circulating IL-6. In the C57BL/6 strain, Prlr^-/- mice displayed similar joint swelling but increased mechanical allodynia compared to Prlr^-+/+ mice.  Consistent with augmented pain, a two-fold enhanced synovial hyperplasia occurred in the absence of the PRLR, although circulating levels of IL-6 were similar between Prlr^-/- and Prlr^-+/+ mice.

Conclusion: Loss of the PRLR correlates with an aggravated AIA phenotype with different symptoms depending on the genetic background. These findings support the protective role of the PRL system in inflammatory arthritis. Work supported by UNAM-Grant IN200312.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/deletion-of-the-prolactin-receptor-aggravates-the-course-of-antigen-induced-arthritis/