Atopic Dermatitis-like Graft-versus-host Disease and Lichen Planus-like Graft-versus-host Disease: Alterations in Skin Barrier Function and Related Molecules.

Abstract:

BACKGROUND:Graft-versus-host disease (GVHD) is a common complication of hematopoietic stem cell transplantation. Skin barrier disruption could induce thymic stromal lymphopoietin (TSLP) expression, and the expression of TSLP was increased in lesions of atopic dermatitis (AD)-like GVHD and lichen planus (LP)-like GVHD. This study attempted to investigate the skin barrier function of AD-like GVHD and LP-like GVHD and possible mechanisms. METHODS:Eighteen AD-like GVHD patients, 12 LP-like GVHD patients, and 14 healthy volunteers were enrolled in this study. Skin biopsy was done in five AD-like GVHD patients, eight LP-like GVHD patients, and eight healthy volunteers. The intensity of pruritus was assessed by visual analog scale itch score and detailed pruritus score. Transepidermal water loss (TEWL) was measured using Tewameter® TM 300. Immunohistochemistry was used to observe the expression of loricrin, involucrin, LL37, and human β-defensins 2 (hBD2) in skin lesions. Western blot analysis was used for analyzing the protein levels of loricrin and involucrin in skin lesions. Real-time polymerase chain reaction was performed to assess the mRNA levels of LL37 and hBD2 in skin lesions. RESULTS:Pruritus score was higher in patients with AD-like GVHD (11.33 ± 5.35) than that of patients with LP-like GVHD (2.58 ± 3.09, P< 0.001). Compared with healthy controls (HCs, 4.52 ± 1.24 g·m-2·h-1), TEWL was increased in AD-like GVHD (26.72 ± 9.02 g·m-2·h-1, P < 0.001) and LP-like GVHD patients (18.78 ± 4.57 g·m-2·h-1, P< 0.001), and expressions of loricrin and involucrin were also increased in skin lesions of AD-like GVHD and LP-like GVHD patients (all P< 0.05). LL37 mRNA expression was decreased in lesions of AD-like GVHD and LP-like GVHD patients (P = 0.005 and P = 0.008, vs. HCs, respectively). hBD2 mRNA expression was increased in skin lesions of AD-like GVHD and LP-like GVHD patients (P = 0.002 and P< 0.001, vs. HCs, respectively). CONCLUSIONS:Skin barrier dysfunction is present in AD-like GVHD and LP-like GVHD. The immunoreactions, but not the congenital defect, are considered to be the primary cause of skin barrier impairment in AD-like GVHD and LP-like GVHD.

journal_name

Chin Med J (Engl)

journal_title

Chinese medical journal

authors

Li K,Mu ZL,Chen X,Wen GD,Zhao Y,Zhang JZ

doi

10.4103/0366-6999.207475

subject

Has Abstract

pub_date

2017-06-20 00:00:00

pages

1459-1466

issue

12

eissn

0366-6999

issn

2542-5641

pii

ChinMedJ_2017_130_12_1459_207475

journal_volume

130

pub_type

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