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Dose-Response Efficacy and Mechanisms of Orally Administered Bifidobacterium breve CCFM683 on IMQ-Induced Psoriasis in Mice.

Xinqi Chen, Yang Chen, Catherine Stanton, Reynolds Paul Ross, Jianxin Zhao et al.
Other Nutrients 2023 19 sitasi
PubMed DOI CC-BY PDF
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Study Design

Jenis Studi
animal_study
Intervensi
Dose-Response Efficacy and Mechanisms of Orally Administered Bifidobacterium breve CCFM683 on IMQ-Induced Psoriasis in Mice. 10^8, 10^9, or 10^10 CFU/day Bifidobacterium breve CCFM683
Pembanding
Placebo
Arah Efek
Positive
Risiko Bias
High

Abstract

This study aimed to investigate the dose-response effect of Bifidobacterium breve CCFM683 on relieving psoriasis and its underlying patterns. Specifically, the expression of keratin 16, keratin 17, and involucrin were substantially decreased by administration of 109 CFU and 1010 CFU per day. Moreover, interleukin (IL)-17 and TNF-α levels were substantially decreased by 109 and 1010 CFU/day. Furthermore, the gut microbiota in mice treated with 109 or 1010 CFU/day was rebalanced by improving the diversity, regulating microbe interactions, increasing Lachnoclostridium, and decreasing Oscillibacter. Moreover, the concentrations of colonic bile acids were positively correlated with the effectiveness of the strain in relieving psoriasis. The gavage dose should be more than 108.42 CFU/day to improve psoriasis according to the dose-effect curve. In conclusion, CCFM683 supplementation alleviated psoriasis in a dose-dependent manner by recovering microbiota, promoting bile acid production, regulating the FXR/NF-κB pathway, diminishing proinflammatory cytokines, regulating keratinocytes, and maintaining the epidermal barrier function. These results may help guide probiotic product development and clinical trials in psoriasis.

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Figures

Tables

Table 2

GeneForward Primer (5′–3′)Reverse Primer (5′–3′)
k1 TGGGAGATTTTCAGGAGGAGGGCCACACTCTTGGAGATGCTC
k10 CTGGCGATGTGAACGTGGAAGTCCCTGAACAGTGCGTCTC
k16 GGTGGCCTCTAACAGTGATCTTGCATACAGTATCTGCCTTTGG
k17 ACCATCCGCCAGTTTACCTCCTACCCAGGCCACTAGCTGA
Lor GCGGATCGTCCCAACAGTATCTGAGAGGAGTAATAGCCCCCT
Ivl ATGTCCCATCAACACACACTGTGGAGTTGGTTGCTTTGCTTG
Flg ATGTCCGCTCTCCTGGAAAGTGGATTCTTCAAGACTGCCTGTA
G-CSF ATGGCTCAACTTTCTGCCCAGCTGACAGTGACCAGGGGAAC
CCL3 TTCTCTGTACCATGACACTCTGCCGTGGAATCTTCCGGCTGTAG
CCL5 GCTGCTTTGCCTACCTCTCCTCGAGTGACAAACACGACTGC
CCL8 TCTACGCAGTGCTTCTTTGCCAAGGGGGATCTTCAGCTTTAGTA
β-actin GGCTGTATTCCCCTCCATCGCCAGTTGGTAACAATGCCATGT

References

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