Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways.

Abstract

Contact dermatitis and psoriasis are skin disorders caused by immune dysregulation, yet much remains unknown about their underlying mechanisms. Ghrelin, a recently discovered novel peptide and potential endogenous anti-inflammatory factor expressed in the epidermis, is involved in skin repair and disease. In this study, we investigated the expression pattern and therapeutic effect of ghrelin in both contact dermatitis and psoriasis mouse models induced by oxazolone (OXA) and imiquimod (IMQ), respectively, and in TNF-α-stimulated RAW264.7 macrophages, NHEKs and skin fibroblasts. Ghrelin expression was reduced in both the OXA-induced contact dermatitis and IMQ-induced psoriasis mouse models. Furthermore, treatment with ghrelin attenuated skin inflammation in both the contact dermatitis and psoriasis mouse models. Mice administered PBS after OXA- or IMQ-induced model generation exhibited typical skin inflammation, whereas ghrelin treatment in these mouse models substantially decreased the dermatitis phenotype. In addition, exogenous ghrelin attenuated the inflammatory reaction induced by TNF-α in RAW264.7 cells. Moreover, ghrelin administration limited activation of NF-κB signaling. In summary, ghrelin may represent a potential molecular target for the prevention and treatment of inflammatory skin diseases, including contact dermatitis and psoriasis.

• Authors: Ruize Qu, Xiaomin Chen, Jing Hu, Yufeng Fu, Jiangfan Peng, Yuhua Li, Jingxi Chen, Peng Li, Long Liu, Jiankang Cao, Wenhan Wang, Cheng Qiu, Linlin Guo, Krasimir Vasilev, Jianying Chen, Gengyin Zhou, Weiwei Li, Yunpeng Zhao
• Journal: Scientific reports (Sci Rep) Vol. 9 Issue 1 Pg. 1348 (02 04 2019) ISSN: 2045-2322 [Electronic] England
• PMID: 30718736 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Ghrelin
• NF-kappa B
• Tumor Necrosis Factor-alpha
• Oxazolone
• Imiquimod

Topics

• Animals
• Dermatitis, Contact (genetics, immunology, pathology)
• Disease Models, Animal
• Fibroblasts (drug effects, metabolism)
• Gene Expression Regulation (drug effects, immunology)
• Ghrelin (genetics)
• Humans
• Imiquimod (toxicity)
• Immune System Diseases (chemically induced, genetics, immunology, pathology)
• Inflammation (chemically induced, genetics, immunology, pathology)
• Mice
• NF-kappa B (genetics)
• Oxazolone (toxicity)
• Psoriasis (chemically induced, genetics, immunology, pathology)
• RAW 264.7 Cells
• Signal Transduction
• Skin (immunology, pathology)
• Tumor Necrosis Factor-alpha (genetics)