Chen Hui-Ling, Zeng Yi-Bin, Zhang Zheng-Yan, Kong Chao-Yue, Zhang Shi-Long, Li Zhan-Ming, Huang Jia-Ting, Xu Ya-Yun, Mao Yu-Qin, Cai Pei-Ran, Han Bing, Wang Wu-Qing, Wang Li-Shun
Center for Traditional Chinese Medicine and Gut Microbiota, Minhang Hospital, Fudan University, Shanghai, 201100, People's Republic of China.
Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan University, Shanghai, 201100, People's Republic of China.
J Inflamm Res. 2021 Nov 24;14:6175-6190. doi: 10.2147/JIR.S337031. eCollection 2021.
Psoriasis is a chronic autoinflammatory skin disease, and its aetiology remains incompletely understood. Recently, gut microbial dysbiosis is found to be tightly associated with psoriasis.
We sought to reveal the causal role of gut microbiota dysbiosis in psoriasis pathogenesis and investigate the protective effect of healthy commensal bacteria against imiquimod -induced psoriasis-like skin response.
By using fecal microbial transplantation (FMT), 16S rRNA gene-based taxonomic profiling and supplement, we have assessed the effect of FMT from healthy individuals on psoriasis-like skin inflammation and associated immune disorders in imiquimod-induced psoriasis mice.
Here, by using psoriasis mice humanized with the stools from healthy donors and psoriasis patients, the imiquimod-induced psoriasis in mice with psoriasis patient stool was found to be significantly aggravated as compared to the mice with healthy donor stools. Further analysis showed fecal microbiota of healthy individuals protected against Treg/Th17 imbalance in psoriasis. Moreover, we found the gut and skin microbiome in mice receipted with gut microbiota of healthy individuals (HD) differed from those of mice receipted with gut microbiota of psoriasis patients (PSD). 16S rRNA sequencing revealed that was greatly enriched in fecal and cutaneous microbiome of HD mice as compared to PSD mice. Intriguingly, supplement with was sufficient to increase the expression of anti-inflammatory gene IL-10, reduce Th17 cells counts and confer resistance to imiquimod-induced inflammation on the mice with gut microbiota dysbiosis.
Our results suggested that the gut microbiota dysbiosis is the potential causal factor for psoriasis and the gut microbiota may serve as promising therapy target for psoriasis patients.
银屑病是一种慢性自身炎症性皮肤病，其病因仍未完全明确。最近，发现肠道微生物群失调与银屑病密切相关。
我们试图揭示肠道微生物群失调在银屑病发病机制中的因果作用，并研究健康共生菌对咪喹莫特诱导的银屑病样皮肤反应的保护作用。
通过粪便微生物移植（FMT）、基于16S rRNA基因的分类分析和补充，我们评估了来自健康个体的FMT对咪喹莫特诱导的银屑病小鼠银屑病样皮肤炎症和相关免疫紊乱的影响。
在此，通过使用用健康供体和银屑病患者粪便人源化的银屑病小鼠，发现与接受健康供体粪便的小鼠相比，接受银屑病患者粪便的小鼠中咪喹莫特诱导的银屑病明显加重。进一步分析表明，健康个体的粪便微生物群可防止银屑病中Treg/Th17失衡。此外，我们发现接受健康个体（HD）肠道微生物群的小鼠的肠道和皮肤微生物组与接受银屑病患者（PSD）肠道微生物群的小鼠不同。16S rRNA测序显示，与PSD小鼠相比， 在HD小鼠的粪便和皮肤微生物组中显著富集。有趣的是，补充 足以增加抗炎基因IL-10的表达，减少Th17细胞计数，并赋予肠道微生物群失调的小鼠对咪喹莫特诱导的炎症的抗性。
我们的结果表明，肠道微生物群失调是银屑病的潜在因果因素，肠道微生物群可能成为银屑病患者有前景的治疗靶点。
