5‐hydroxytryptophan attenuates imiquimod‐induced psoriasiform dermatitis probably through inhibition of <scp>IL</scp>‐17A production and keratinocyte activation

Hsu, Peng-Yang; Yang, Hsin-Chia; Yang, Tao-Hsiang; Su, Chih‐Ying

doi:10.1111/exd.13781

Cited by 6 publications

(3 citation statements)

References 52 publications

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“…The administration of 5-HTP via oral gavage occurred daily at doses of 7.5 mg/kg, 15 mg/kg, and 30 mg/kg for the low, medium, and high dose groups, respectively. These dosages were selected based on their efficacious use in prior studies [19][20][21].…”

Section: Cell Culture and Animals Treatmentsmentioning

confidence: 99%

5-Hydroxytryptophan acts as a gap junction inhibitor to limit the spread of chemotherapy-induced cardiomyocyte injury and mitochondrial dysfunction

Sun,

Lu,

Zhang

et al. 2024

Aging

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Anthracycline chemotherapeutics like doxorubicin (DOX) are widely used against various cancers but are accompanied by severe cardiotoxic effects that can lead to heart failure. Through whole transcriptome sequencing and pathological tissue analysis in a murine model, our study has revealed that DOX impairs collagen expression in the early phase, causing extracellular matrix anomalies that weaken the mechanical integrity of the heart. This results in ventricular wall thinning and dilation, exacerbating cardiac dysfunction. In this work, we have identified 5-hydroxytryptophan (5-HTP) as a potent inhibitor of gap junction communication. This inhibition is key to limiting the spread of DOX-induced cardiotoxicity. Treatment with 5-HTP effectively countered the adverse effects of DOX on the heart, preserving ventricular structure and ejection fraction. Moreover, 5-HTP enhanced mitochondrial respiratory function, as shown by the O2k mitochondrial function assay, by improving mitochondrial complex activity and ATP production. Importantly, the cardioprotective benefits of 5-HTP did not interfere with DOX’s ability to combat cancer. These findings shed light on the cardiotoxic mechanisms of DOX and suggest that 5-HTP could be a viable strategy to prevent heart damage during chemotherapy, offering a foundation for future clinical development. This research opens the door for 5-HTP to be considered a dual-purpose agent that can protect the heart without compromising the oncological efficacy of anthracycline chemotherapy.

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Section: Cell Culture and Animals Treatmentsmentioning

confidence: 99%

5-Hydroxytryptophan acts as a gap junction inhibitor to limit the spread of chemotherapy-induced cardiomyocyte injury and mitochondrial dysfunction

Sun,

Lu,

Zhang

et al. 2024

Aging

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“…This effect is attributed to its capacity to restrain the differentiation of CD4+ T cells producing IFN-γ and IL-17A, alongside reducing the synthesis of correlated cytokines like TNF-α, IL-6, IL-17A, and IFN-γ in splenic cells. Furthermore, the presence of 5(OH)Trp weakens the expression intensity of t-bet, RORγt, and p-STAT3 in stimulated splenic cells ( 113 ).…”

Section: Regulation Of Amino Acid Metabolism On T Cell In Psoriasismentioning

confidence: 99%

Metabolic influences on T cell in psoriasis: a literature review

Su,

Zhao,

Zhang

et al. 2023

Front. Immunol.

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Psoriasis is a systemic inflammatory disease that frequently coexists with various other conditions, such as essential hypertension, diabetes, metabolic syndrome, and inflammatory bowel disease. The association between these diseases may be attributed to shared inflammatory pathways and abnormal immunomodulatory mechanisms. Furthermore, metabolites also play a regulatory role in the function of different immune cells involved in psoriasis pathogenesis, particularly T lymphocytes. In this review, we have summarized the current research progress on T cell metabolism in psoriasis, encompassing the regulation of metabolites in glucose metabolism, lipid metabolism, amino acid metabolism, and other pathways within T cells affected by psoriasis. We will also explore the interaction and mechanism between psoriatic metabolites and immune cells. Moreover, we further discussed the research progress of metabolomics in psoriasis to gain a deeper understanding of its pathogenesis and identify potential new therapeutic targets through identification of metabolic biomarkers associated with this condition.

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“…The first rate-limiting reaction of the 5-HT pathway produces 5-hydroxytryptophan (5 (OH)Trp), another AHR agonist [143]. Treatment with 5 (OH)Trp inhibits IMQ-induced psoriasiform dermatitis in mice and control activation in keratinocytes and splenocytes [144] (Table 1). The serum levels of 5-HT are elevated in psoriatic patients with anxiety, correlate with disease severity, and decrease after treatment [145,146].…”

Section: Endogenous L-tryptophan-derived Ahr Ligandsmentioning

confidence: 99%

Role of AHR Ligands in Skin Homeostasis and Cutaneous Inflammation

Fernández‐Gallego

Sánchez‐Madrid

Cibrián

2021

Cells

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Aryl hydrocarbon receptor (AHR) is an important regulator of skin barrier function. It also controls immune-mediated skin responses. The AHR modulates various physiological functions by acting as a sensor that mediates environment–cell interactions, particularly during immune and inflammatory responses. Diverse experimental systems have been used to assess the AHR’s role in skin inflammation, including in vitro assays of keratinocyte stimulation and murine models of psoriasis and atopic dermatitis. Similar approaches have addressed the role of AHR ligands, e.g., TCDD, FICZ, and microbiota-derived metabolites, in skin homeostasis and pathology. Tapinarof is a novel AHR-modulating agent that inhibits skin inflammation and enhances skin barrier function. The topical application of tapinarof is being evaluated in clinical trials to treat psoriasis and atopic dermatitis. In the present review, we summarize the effects of natural and synthetic AHR ligands in keratinocytes and inflammatory cells, and their relevance in normal skin homeostasis and cutaneous inflammatory diseases.

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5‐hydroxytryptophan attenuates imiquimod‐induced psoriasiform dermatitis probably through inhibition of IL‐17A production and keratinocyte activation

Cited by 6 publications

References 52 publications

5-Hydroxytryptophan acts as a gap junction inhibitor to limit the spread of chemotherapy-induced cardiomyocyte injury and mitochondrial dysfunction

5-Hydroxytryptophan acts as a gap junction inhibitor to limit the spread of chemotherapy-induced cardiomyocyte injury and mitochondrial dysfunction

Metabolic influences on T cell in psoriasis: a literature review

Role of AHR Ligands in Skin Homeostasis and Cutaneous Inflammation

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