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  3. Canthaxanthin ameliorates atopic dermatitis in mice by suppressing Th2 immune response

Canthaxanthin ameliorates atopic dermatitis in mice by suppressing Th2 immune response

  • Int Immunopharmacol. 2025 Feb 6:147:113975. doi: 10.1016/j.intimp.2024.113975.
Shuying Peng 1,  Lu Yu 2,  Mingxin Jiang 3,  Sihang Cao 1,  Hong Wang 4,  Xiao Lu 5,  Yihao Tao 6,  Jia Zhou 5,  Ledong Sun 7,  Daming Zuo 8
Affiliations

Affiliations

  • 1 Institute of Molecular Immunology, Key Laboratory of Infectious Diseases Research in South China, Ministry of Education, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong 510515, China; Guangdong Province Key Laboratory of Proteomics, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
  • 2 Institute of Molecular Immunology, Key Laboratory of Infectious Diseases Research in South China, Ministry of Education, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Blood Transfusion, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, China.
  • 3 Institute of Molecular Immunology, Key Laboratory of Infectious Diseases Research in South China, Ministry of Education, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong 510515, China.
  • 4 Institute of Molecular Immunology, Key Laboratory of Infectious Diseases Research in South China, Ministry of Education, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong 510515, China; Guangdong Medical Products Administration Key Laboratory for Research and Evaluation of Drugs for Inflammatory Diseases, Department of Dermatology, the Fifth Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong 510900, China.
  • 5 Guangdong Province Key Laboratory of Proteomics, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
  • 6 Veritas Collegiate Academy, 935 23rd St S, Arlington, VA 22202-2422, United States.
  • 7 Guangdong Medical Products Administration Key Laboratory for Research and Evaluation of Drugs for Inflammatory Diseases, Department of Dermatology, the Fifth Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong 510900, China. Electronic address: sunledong126@126.com.
  • 8 Institute of Molecular Immunology, Key Laboratory of Infectious Diseases Research in South China, Ministry of Education, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: zdaming@smu.edu.cn.
PMID: 39787760 DOI: 10.1016/j.intimp.2024.113975
Abstract

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder characterized by intense pruritus and complex immunopathogenic mechanisms. Recent evidence has highlighted the critical link between dysregulated intestinal microecology and altered immune responses in AD progression. As essential components of the intestinal microenvironment, metabolites play pivotal roles in various physiological processes. Through metabolomic profiling in an AD mouse model, we identified a significant reduction in canthaxanthin (CTX), a bacterial-derived metabolite naturally present in many foods, in AD mice compared to healthy controls. To investigate the therapeutic potential of CTX, we established an AD model by repeatedly applying 2,4-dinitrochlorobenzene (DNCB) to the ears and dorsal skin of mice, successfully inducing AD-like symptoms and lesions. Notably, oral administration of CTX significantly attenuated skin inflammation and reduced serum IgE levels in this DNCB-induced AD model. Both in vivo and in vitro studies demonstrated that CTX treatment effectively suppressed Th2 immune responses. Mechanistically, we found that CTX significantly inhibited the activation of the JAK2-STAT6 signaling pathway in Th2-polarized T cells. Our findings not only demonstrate the therapeutic efficacy of CTX in AD but also elucidate its molecular mechanism in modulating T helper cell subset balance. These insights suggest that CTX could serve as a promising therapeutic agent for AD and potentially Other Th2 response-mediated immune disorders.

Keywords

Atopic dermatitis; Canthaxanthin; Gut metabolite; STAT6; Th2 cells.

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