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Diverse expression of TNF‐α and CCL27 in serum and blister of Stevens–Johnson syndrome/toxic epidermal necrolysis
Author(s) -
Wang Fang,
Ye Yanting,
Luo ZeYu,
Gao Qian,
Luo DiQing,
Zhang Xingqi
Publication year - 2018
Publication title -
clinical and translational allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.979
H-Index - 37
ISSN - 2045-7022
DOI - 10.1186/s13601-018-0199-6
Subject(s) - toxic epidermal necrolysis , medicine , tumor necrosis factor alpha , pathogenesis , immunology , cytokine , dermatology
Background The pathogenesis of Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) is not fully understood. Our previous study reported that chemokine CCL27 was overexpressed in serum of SJS/TEN patients. The objective of this study was to investigate the levels of CCL27 and TNF‐α in serum and blister fluid from patients with SJS/TEN during the acute stage or resolution phase. Methods A total of 27 patients with SJS/TEN and 39 healthy donors were recruited to the study. Serum and vesicular levels of CCL27 and TNF‐α were determined by enzyme‐linked immunosorbent assays. Results Serum levels of CCL27 and TNF‐α were significantly elevated in patients with SJS/TEN during the acute stage as compared to the resolution phase and also compared with levels observed in normal controls ( P  = 0.001/< 0.001; P  = 0.012/< 0.001). Serum TNF‐α levels were significantly higher in patients with SJS/TEN during the resolution phase compared with normal controls ( P  < 0.001). Serum CCL27 levels were positively correlated with TNF‐α levels during the acute stage ( r s  = 0.660; P  < 0.001). Blister fluid exhibited much lower CCL27 levels than serum did during the acute stage ( P  = 0.008). TNF‐α levels were much higher in vesicles in contrast to serum from acute stage ( P  = 0.040) as well as serum from resolution phase ( P  = 0.029). Conclusions Our study demonstrated roles of CCL27 and TNF‐α in promoting the course of SJS/TEN. CCL27 may act early in the course of disease, via the circulation, whereas TNF‐α acts throughout the course of disease, in skin lesions.

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