Abstract
Psoriasis is a chronic inflammatory skin disease characterized by accelerated tumor necrosis factor-α/interleukin-23/interleukin-17 axis, hyperproliferation and abnormal differentiation of epidermal keratinocytes. Psoriasis patients are frequently associated with obesity, diabetes, dyslipidemia, cardiovascular diseases, or inflammatory bowel diseases. Psoriasis patients often show unbalanced dietary habits such as higher intake of fat and lower intake of fish or dietary fibers, compared to controls. Such dietary habits might be related to the incidence and severity of psoriasis. Nutrition influences the development and progress of psoriasis and its comorbidities. Saturated fatty acids, simple sugars, red meat, or alcohol exacerbate psoriasis via the activation of nucleotide-binding domain, leucine-rich repeats containing family, pyrin domain-containing-3 inflammasome, tumor necrosis factor-α/interleukin-23/interleukin-17 pathway, reactive oxygen species, prostanoids/leukotrienes, gut dysbiosis or suppression of regulatory T cells, while n-3 polyunsaturated fatty acids, vitamin D, vitamin B12, short chain fatty acids, selenium, genistein, dietary fibers or probiotics ameliorate psoriasis via the suppression of inflammatory pathways above or induction of regulatory T cells. Psoriasis patients are associated with dysbiosis of gut microbiota and the deficiency of vitamin D or selenium. We herein present the update information regarding the stimulatory or regulatory effects of nutrients or food on psoriasis and the possible alleviation of psoriasis by nutritional strategies.
Highlights
Psoriasis is a chronic inflammatory skin disease characterized by an accelerated tumor necrosis factor-α (TNF-α)/interleukin-23 (IL-23)/IL-17 axis, and hyperproliferation and aberrant differentiation of epidermal keratinocytes [1]
Oral administration of genistein in psoriasis patients for 8 weeks impaired the transcription of genes overexpressed in psoriasis, CXCL10, IL-6, signal transducer and activator of transcription 3 (STAT3), NFKB1, CCL4 while stimulated the transcription of gene repressed in psoriasis, IL-1RN in peripheral blood cells or lesional skin [75]
Several studies show that supplementation with probiotics ameliorates skin inflammation in psoriasis model mice: Lactobacillus pentosus GMNL-77 administration reduced skin scores in IMQ-induced psoriasiform dermatitis and decreased the expression of TNF-α, IL-6, IL-23, IL-17A, IL-17F, and IL-22 in the skin lesions and decreased the numbers of Th17 and Th22 cells in the spleen [102]
Summary
Psoriasis is a chronic inflammatory skin disease characterized by an accelerated tumor necrosis factor-α (TNF-α)/interleukin-23 (IL-23)/IL-17 axis, and hyperproliferation and aberrant differentiation of epidermal keratinocytes [1]. TP-deficient mice showed the reduced inflammation with decreased number of γδT17 cells in the IMQ-induced dermatitis [19]. Another prostanoid, prostaglandin E2 (PGE2) promotes the IMQ-induced psoriasiform dermatitis; PGE2 produced by fibroblasts promotes the production of IL-23 in dendritic cells (DCs) [20]. Resolvin E1 antagonized the LTB4-induced IL-23 production and migration of DCs, Th17 cells and γδT17 cells These antagonistic effects of resolving E1 were mediated by binding to LTB4 receptor, BLT1. SCFAs, especially butyrate, induce the differentiation of thymic Tregs by promoting the expression of a transcription factor autoimmune regulator (Aire) in medullary thymic epithelial cells via GPR41 [31]. Topical application of sodium butyrate in IMQ-induced psoriasiform dermatitis, reduced the inflammation, downregulated IL-17 expression, and induced IL-10 and Foxp transcripts [33]. Sodium butyrate enhanced terminal differentiation of keratinocytes and downregulated their proliferation via inhibiting histone deacetylase [35]: sodium butyrate in vitro increased the mRNA levels of filaggrin and transglutaminase A, and promoted cornified envelope formation in normal human keratinocytes [35]
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