5‐hydroxytryptophan attenuates imiquimod‐induced psoriasiform dermatitis probably through inhibition of IL‐17A production and keratinocyte activation
Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that 5‐hydroxytryptophan (5(OH)Trp), a tryptophan metabolite, alleviated collagen‐induced arthritis and suppressed cytokine production. In this study, we evaluated...
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| Published in | Experimental dermatology Vol. 27; no. 11; pp. 1273 - 1279 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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01.11.2018
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| Abstract | Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that 5‐hydroxytryptophan (5(OH)Trp), a tryptophan metabolite, alleviated collagen‐induced arthritis and suppressed cytokine production. In this study, we evaluated the effects of 5(OH)Trp in a mouse model for psoriasiform dermatitis, induced by imiquimod (IMQ). We showed that 5(OH)Trp significantly reduced the cumulative scores, epidermal thickness and ki‐67 expression in the skin. In addition, 5(OH)Trp decreased local and systemic inflammation. Moreover, 5(OH)Trp significantly inhibited keratinocyte activation with decrease in IL‐6 production and p‐Erk1/2 and p‐STAT3 expression. 5(OH)Trp also inhibited the differentiation of IFN‐γ‐ and IL‐17A‐expressing CD4+ T cells and related cytokine production (TNF‐α, IL‐6, IL‐17A and IFN‐γ) in splenocytes. In conclusion, 5(OH)Trp can inhibit imiquimod‐induced psoriasiform dermatitis in mice and inhibit activation in keratinocytes and splenocytes. |
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| AbstractList | Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that 5‐hydroxytryptophan (5(OH)Trp), a tryptophan metabolite, alleviated collagen‐induced arthritis and suppressed cytokine production. In this study, we evaluated the effects of 5(OH)Trp in a mouse model for psoriasiform dermatitis, induced by imiquimod (IMQ). We showed that 5(OH)Trp significantly reduced the cumulative scores, epidermal thickness and ki‐67 expression in the skin. In addition, 5(OH)Trp decreased local and systemic inflammation. Moreover, 5(OH)Trp significantly inhibited keratinocyte activation with decrease in IL‐6 production and p‐Erk1/2 and p‐STAT3 expression. 5(OH)Trp also inhibited the differentiation of IFN‐γ‐ and IL‐17A‐expressing CD4+ T cells and related cytokine production (TNF‐α, IL‐6, IL‐17A and IFN‐γ) in splenocytes. In conclusion, 5(OH)Trp can inhibit imiquimod‐induced psoriasiform dermatitis in mice and inhibit activation in keratinocytes and splenocytes. Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that 5‐hydroxytryptophan (5( OH )Trp), a tryptophan metabolite, alleviated collagen‐induced arthritis and suppressed cytokine production. In this study, we evaluated the effects of 5( OH )Trp in a mouse model for psoriasiform dermatitis, induced by imiquimod ( IMQ ). We showed that 5( OH )Trp significantly reduced the cumulative scores, epidermal thickness and ki‐67 expression in the skin. In addition, 5( OH )Trp decreased local and systemic inflammation. Moreover, 5( OH )Trp significantly inhibited keratinocyte activation with decrease in IL ‐6 production and p‐Erk1/2 and p‐ STAT 3 expression. 5( OH )Trp also inhibited the differentiation of IFN ‐γ‐ and IL ‐17A‐expressing CD 4 + T cells and related cytokine production ( TNF ‐α, IL ‐6, IL ‐17A and IFN ‐γ) in splenocytes. In conclusion, 5( OH )Trp can inhibit imiquimod‐induced psoriasiform dermatitis in mice and inhibit activation in keratinocytes and splenocytes. Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that 5-hydroxytryptophan (5(OH)Trp), a tryptophan metabolite, alleviated collagen-induced arthritis and suppressed cytokine production. In this study, we evaluated the effects of 5(OH)Trp in a mouse model for psoriasiform dermatitis, induced by imiquimod (IMQ). We showed that 5(OH)Trp significantly reduced the cumulative scores, epidermal thickness and ki-67 expression in the skin. In addition, 5(OH)Trp decreased local and systemic inflammation. Moreover, 5(OH)Trp significantly inhibited keratinocyte activation with decrease in IL-6 production and p-Erk1/2 and p-STAT3 expression. 5(OH)Trp also inhibited the differentiation of IFN-γ- and IL-17A-expressing CD4 T cells and related cytokine production (TNF-α, IL-6, IL-17A and IFN-γ) in splenocytes. In conclusion, 5(OH)Trp can inhibit imiquimod-induced psoriasiform dermatitis in mice and inhibit activation in keratinocytes and splenocytes. Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that 5-hydroxytryptophan (5(OH)Trp), a tryptophan metabolite, alleviated collagen-induced arthritis and suppressed cytokine production. In this study, we evaluated the effects of 5(OH)Trp in a mouse model for psoriasiform dermatitis, induced by imiquimod (IMQ). We showed that 5(OH)Trp significantly reduced the cumulative scores, epidermal thickness and ki-67 expression in the skin. In addition, 5(OH)Trp decreased local and systemic inflammation. Moreover, 5(OH)Trp significantly inhibited keratinocyte activation with decrease in IL-6 production and p-Erk1/2 and p-STAT3 expression. 5(OH)Trp also inhibited the differentiation of IFN-γ- and IL-17A-expressing CD4+ T cells and related cytokine production (TNF-α, IL-6, IL-17A and IFN-γ) in splenocytes. In conclusion, 5(OH)Trp can inhibit imiquimod-induced psoriasiform dermatitis in mice and inhibit activation in keratinocytes and splenocytes.Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that 5-hydroxytryptophan (5(OH)Trp), a tryptophan metabolite, alleviated collagen-induced arthritis and suppressed cytokine production. In this study, we evaluated the effects of 5(OH)Trp in a mouse model for psoriasiform dermatitis, induced by imiquimod (IMQ). We showed that 5(OH)Trp significantly reduced the cumulative scores, epidermal thickness and ki-67 expression in the skin. In addition, 5(OH)Trp decreased local and systemic inflammation. Moreover, 5(OH)Trp significantly inhibited keratinocyte activation with decrease in IL-6 production and p-Erk1/2 and p-STAT3 expression. 5(OH)Trp also inhibited the differentiation of IFN-γ- and IL-17A-expressing CD4+ T cells and related cytokine production (TNF-α, IL-6, IL-17A and IFN-γ) in splenocytes. In conclusion, 5(OH)Trp can inhibit imiquimod-induced psoriasiform dermatitis in mice and inhibit activation in keratinocytes and splenocytes. |
| Author | Su, Che‐Chun Hsu, Peng‐Yang Yang, Tao‐Hsiang Yang, Hui‐Ju |
| Author_xml | – sequence: 1 givenname: Peng‐Yang surname: Hsu fullname: Hsu, Peng‐Yang organization: Changhua Christian Hospital – sequence: 2 givenname: Hui‐Ju surname: Yang fullname: Yang, Hui‐Ju organization: Changhua Christian Hospital – sequence: 3 givenname: Tao‐Hsiang surname: Yang fullname: Yang, Tao‐Hsiang organization: Changhua Christian Hospital – sequence: 4 givenname: Che‐Chun orcidid: 0000-0001-5230-0126 surname: Su fullname: Su, Che‐Chun email: 115025@cch.org.tw, jamesccsu67@gmail.com organization: Changhua Christian Hospital |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30221419$$D View this record in MEDLINE/PubMed |
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| Keywords | psoriasiform dermatitis IL-17A imiquimod 5-hydroxytryptophan |
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| Snippet | Psoriasis is a chronic autoimmune disease with keratinocyte activation and lymphocyte infiltration in the skin. Our previous study found that... |
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| SubjectTerms | 5‐hydroxytryptophan Arthritis CD4 antigen Cell activation Collagen Cytokines Dermatitis IL‐17A Imiquimod Interferon Keratinocytes Lymphocytes T psoriasiform dermatitis Psoriasis Splenocytes Stat3 protein Tryptophan Tumor necrosis factor |
| Title | 5‐hydroxytryptophan attenuates imiquimod‐induced psoriasiform dermatitis probably through inhibition of IL‐17A production and keratinocyte activation |
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