In:
Experimental Dermatology, Wiley, Vol. 27, No. 11 ( 2018-11), p. 1245-1253
Abstract:
Human prolactin ( PRL ) is a well‐known hormone for pituitary of lactation and reproduction, but it also has immunostimulatory effect in some inflammatory or autoimmune diseases including psoriasis, which has not been well elucidated. This study aimed to determine the relationship between PRL and psoriasis through clinical case‐control studies, and explore the function of PRL in the pathogenesis of imiquimod ( IMQ )‐induced psoriasis‐like mouse model. Serum from patients with psoriasis vulgaris (PsV), patients with erythrodermic psoriasis, and healthy controls ( HC s) were collected for PRL test. Skin biopsies were collected for PRL , PRL receptors ( PRLR s), cytokines mRNA level determination, PRL immunohistochemistry and PRL Western blotting. Mice were divided into four groups (each n = 6): control group ( CON ), IMQ group, anti‐ PRL group and solvent group. Anti‐ PRL group and solvent group mice were treated with PRL antagonist (cabergoline) and the solvent (0.25% methylcellulose) separately. The serum PRL level of PsV patients was significantly higher than that of HC s ( P 〈 0.001). Compared with HC s, the mRNA levels of PRL and Th1/Th17 cytokines in skin lesions increased significantly ( P 〈 0.05), and the PRL protein level was also significantly elevated in the epidermis and dermis of PsV patients. In IMQ ‐induced psoriasis‐like mouse model, the mRNA and protein levels of PRL in skin lesions were significantly higher than CON group ( P 〈 0.01). Comparing to solvent group, serum PRL level and PRL , cytokines mRNA levels in skin lesions all decreased significantly and the skin inflammatory condition was also alleviated obviously in anti‐ PRL group. This study suggests that local production of PRL is the main resource of PRL in skin lesions and may play an important role in skin inflammatory of psoriasis.
Type of Medium:
Online Resource
ISSN:
0906-6705
,
1600-0625
DOI:
10.1111/exd.2018.27.issue-11
Language:
English
Publisher:
Wiley
Publication Date:
2018
detail.hit.zdb_id:
2026228-0
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