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Review
. 2020 Jul 29;21(15):5405.
doi: 10.3390/ijms21155405.

Nutrition and Psoriasis

Naoko Kanda  1 , Toshihiko Hoashi  2 , Hidehisa Saeki  2
Affiliations
Review

Nutrition and Psoriasis

Naoko Kanda et al. Int J Mol Sci. .

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.

Keywords: dysbiosis; interleukin-17; n-3 polyunsaturated fatty acid; nutrition; psoriasis; regulatory T cell; saturated fatty acid; short chain fatty acid; vitamin D.

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Conflict of interest statement

There are no conflict of interest.

Figures

Figure 1
Figure 1
Tumor necrosis factor(TNF-α)/interleukin-23 (IL-23)/IL-17 axis in the pathogenesis of psoriasis. Dendritic cells activated by various stimuli in the lesional skin secrete TNF-α which acts on themselves in an autocrine manner and induces IL-23 secretion. The IL-23 promotes the proliferation and survival of Th17 cells. The activated Th17 cells overproduce IL-17A or IL-22 which act on keratinocytes and induce their proliferation and production of TNF-α, antimicrobial peptides, or chemokines C-X-C motif ligand 1 (CXCL1)/8, C-C-motif ligand 20 (CCL20), which further recruit neutrophils, lymphocytes, or monocytes. The activation of keratinocytes by IL-17A or TNF-α induces the expression of keratins 6 and 16, which are associated with acanthosis and reduced turnover time in the epidermis.
Figure 2
Figure 2
Saturated fatty acids (SFAs), red meat, simple sugars, or alcohol promote the development and progress of psoriasis and its comorbidities via the activation of nucleotide-binding domain, leucine-rich repeats containing family, pyrin domain-containing-3 (NLRP3) inflammasome cascade, TNF-α/IL-23/IL-17 axis, generation of reactive oxygen species (ROS), prostanoids/leukotrienes, gut dysbiosis, or suppression of regulatory T cells (Tregs). In contrast, n-3 polyunsaturated fatty acids (PUFAs), vitamin D, vitamin B12, dietary fibers, short chain fatty acids (SCFAs), genistein, selenium or probiotics ameliorate psoriasis or its comorbidities via the suppression of above inflammatory signaling pathways or the induction of Tregs. MI, myocardial infarction; IBD, inflammatory bowel disease; PGE2, prostaglandin E2; TXA2, thromboxane A2; LTB4, leukotriene B4.
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