PMID- 37545106
OWN - NLM
STAT- MEDLINE
DCOM- 20231116
LR  - 20231116
IS  - 1600-0781 (Electronic)
IS  - 0905-4383 (Linking)
VI  - 39
IP  - 6
DP  - 2023 Nov
TI  - Role of interleukin-36gamma induced by ultraviolet radiation in chronic actinic 
      dermatitis.
PG  - 598-606
LID - 10.1111/phpp.12903 [doi]
AB  - BACKGROUND: Chronic actinic dermatitis (CAD) is an immune-mediated 
      photodermatosis characterized by a high eosinophil count and total immunoglobulin 
      E (IgE) in the peripheral blood of patients. At present, however, the reasons for 
      their elevation remain unclear. OBJECTIVE: The current study aimed to detect 
      changes in inflammatory cytokines in CAD and explore their role in this disease. 
      METHODS: Enzyme-linked immunosorbent assay and Luminex assay were conducted to 
      measure inflammatory factor levels. Immunohistochemical analysis and quantitative 
      real-time polymerase chain reaction were performed to evaluate the expression 
      levels of interleukin-36gamma (IL-36gamma), IL-8, chemokine (C-C motif) ligand 17 
      (CCL17), and CCL18. CCK8 kits were used to assess cell proliferation. 
      Immunofluorescence was used to detect nuclear factor kappaB (NF-kappaB) p65 nuclear 
      translocation. Western blot analysis was performed to detect the protein 
      expression level of phosphorylated NF-kappaB (p-NF-kappaB) p65. Hematoxylin and eosin and 
      Masson trichrome staining were applied to observe histological changes in a 
      chronic photo-damaged mouse model. RESULTS: Eosinophils, total IgE, IL-36gamma, IL-8, 
      tumor necrosis factor alpha, CCL17, and CCL18 were elevated in CAD. Of note, IL-36gamma 
      promoted the proliferation of eosinophilic cells (EOL-1) and the production of 
      IgE in peripheral blood mononuclear cells. IL-36gamma also promoted the production of 
      IL-8 and CCL18 in immortalized human keratinocytes (HaCaT cells), while 
      ultraviolet radiation (UVR)-induced IL-36gamma via activation of the NF-kappaB signaling 
      pathway. CONCLUSIONS: IL-36gamma was involved in the pathogenesis of CAD and UVR 
      contributed to the production of IL-36gamma, which may provide a novel therapeutic 
      target for CAD.
CI  - (c) 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Wang, Li
AU  - Wang L
AD  - Department of Dermatology, Wuhan No. 1 Hospital, Hubei, China.
AD  - Department of Dermatology, First Affiliated Hospital of Kunming Medical 
      University, Kunming, China.
FAU - Tu, Yunhua
AU  - Tu Y
AD  - Department of Dermatology, First Affiliated Hospital of Kunming Medical 
      University, Kunming, China.
AD  - Department of Dermatology, Second People's Hospital of Guiyang, Guiyang, China.
FAU - Wu, Wenjuan
AU  - Wu W
AUID- ORCID: 0000-0002-1138-9096
AD  - Department of Dermatology, First Affiliated Hospital of Kunming Medical 
      University, Kunming, China.
FAU - Tu, Ying
AU  - Tu Y
AD  - Department of Dermatology, First Affiliated Hospital of Kunming Medical 
      University, Kunming, China.
FAU - Yang, Zhenghui
AU  - Yang Z
AD  - Department of Dermatology, First Affiliated Hospital of Kunming Medical 
      University, Kunming, China.
FAU - Chai, Yanjie
AU  - Chai Y
AD  - Department of Dermatology, First Affiliated Hospital of Kunming Medical 
      University, Kunming, China.
FAU - Yang, Xinwang
AU  - Yang X
AD  - Department of Anatomy and Histology & Embryology, Faculty of Basic Medical 
      Science, Kunming Medical University, Kunming, Yunnan, China.
FAU - He, Li
AU  - He L
AD  - Department of Dermatology, First Affiliated Hospital of Kunming Medical 
      University, Kunming, China.
LA  - eng
GR  - Clinical Medical Center for Dermatology and Immunology of Yunnan Province 
      (2019ZF012)/
GR  - Guiyang Science and Technology Planning Project [2023 48-26]/
GR  - National Natural Science Foundation of China [82260625]/
GR  - Science and Technology Plan of Guiyang Municipal Health Bureau [No. 2020-002]/
GR  - Science and Technology Program of Guizhou Provincial Health Bureau 
      [gzwkj2021-155]/
GR  - Yunnan Provincial Postdoctoral Science Foundation/
GR  - 202301AS070036/Key Program of Yunnan Fundamental Research Project/
GR  - 202301AS070001-301/Outstanding Youth Program of Yunnan Applied Baisc Reaearch 
      Project-Kunming Medical University Union Foundation/
PT  - Journal Article
DEP - 20230806
PL  - England
TA  - Photodermatol Photoimmunol Photomed
JT  - Photodermatology, photoimmunology & photomedicine
JID - 9013641
RN  - 0 (NF-kappa B)
RN  - 0 (Interleukin-8)
RN  - 0 (Interleukins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Humans
MH  - *Ultraviolet Rays/adverse effects
MH  - NF-kappa B/metabolism
MH  - Interleukin-8
MH  - Leukocytes, Mononuclear
MH  - Interleukins
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - *Photosensitivity Disorders
MH  - Immunoglobulin E
OTO - NOTNLM
OT  - IL-36gamma
OT  - IgE
OT  - chronic actinic dermatitis
OT  - eosinophils
OT  - ultraviolet
EDAT- 2023/08/07 06:41
MHDA- 2023/11/16 06:45
CRDT- 2023/08/07 01:03
PHST- 2023/06/20 00:00 [revised]
PHST- 2023/04/30 00:00 [received]
PHST- 2023/07/14 00:00 [accepted]
PHST- 2023/11/16 06:45 [medline]
PHST- 2023/08/07 06:41 [pubmed]
PHST- 2023/08/07 01:03 [entrez]
AID - 10.1111/phpp.12903 [doi]
PST - ppublish
SO  - Photodermatol Photoimmunol Photomed. 2023 Nov;39(6):598-606. doi: 
      10.1111/phpp.12903. Epub 2023 Aug 6.