Abstract

Psoriasis is an immune-mediated systemic disease that may be treated with probiotics. In this study, probiotic strains that could or could not decrease interleukin (IL)-17 levels were applied to imiquimod (IMQ)-induced psoriasis-like mice via oral administration. Bifidobacterium adolescentis CCFM667, B. breve CCFM1078, Lacticaseibacillus paracasei CCFM1074, and Limosilactobacillus reuteri CCFM1132 ameliorated psoriasis-like pathological characteristics and suppressed the release of IL-23/T helper cell 17 (Th17) axis-related inflammatory cytokines, whereas B. animalis CCFM1148, L. paracasei CCFM1147, and L. reuteri CCFM1040 neither alleviated the pathological characteristics nor reduced the levels of inflammatory cytokines. All effective strains increased the contents of short-chain fatty acids, which were negatively correlated with the levels of inflammatory cytokines. By performing 16S rRNA gene sequencing, the diversity of gut microbiota in psoriasis-like mice was found to decrease, but all effective strains made some specific changes to the composition of gut microbiota compared to the ineffective strains. Furthermore, except for B. breve CCFM1078, all other effective strains decreased the abundance of the family Rikenellaceae, which was positively correlated with psoriasis-like pathological characteristics and was negatively correlated with propionate levels. These findings demonstrated effects of strain-specificity, and how probiotics ameliorated psoriasis and provide new possibilities for the treatment of psoriasis.

Highlights

  • Psoriasis is a skin disease with erythema and scales as the main clinical manifestations.Psoriasis was originally thought to be a disease of epidermal keratinocytes, but is considered one of the most common immune-mediated diseases [1]

  • It was found that B. adolescentis CCFM667 reduced IL-17 levels in mice did ameliorate psoriasis, while B. animalis CCFM1148 and L. paracasei CCFM1147 failed to reduce IL-17 levels and did not

  • In the IL-23/T helper cell 17 (Th17) axis, IL-23 induces the differentiation of Th17 cells and promotes the secretion of IL-22 and IL-17, which eventually leads to the aggravation of psoriasis [39]

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Summary

Introduction

Psoriasis is a skin disease with erythema and scales as the main clinical manifestations.Psoriasis was originally thought to be a disease of epidermal keratinocytes, but is considered one of the most common immune-mediated diseases [1]. Psoriasis is a skin disease with erythema and scales as the main clinical manifestations. It has been recently confirmed that the pathogenesis of psoriasis is not due to a single cause, and involves many aspects, including genetic, immunological, environmental, and other factors [6]. Several abnormalities occur during the development of psoriasis, including in antigen presentation, activation of the nuclear factor kappa-B signalling pathway, T helper (Th) cells population differentiation (especially Th17 cells), and enhancement of IL-17 responses [6,8]. IL-23 drives the differentiation of Th17 cells, and Th17 cells subsequently produce IL-22 and IL-17 [9] These inflammatory cytokines, especially IL-17, accelerate the development of psoriasis [10]. Many kin of biologics, including anti-IL-12/23p40 antibody and IL-17 inhibitors [11], have been used to treat psoriasis. We hypothesised that probiotics that suppress the release of IL-17 may be used to treat psoriasis

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