Gut microbiota facilitate chronic spontaneous urticaria.
Gut microbiota facilitate chronic spontaneous urticaria.
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DOI：
10.1038/s41467-023-44373-x
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发表时间：
2024-01-02
影响因子：
16.6
通讯作者：
Li, Jie
中科院分区：
文献类型：
--
作者：
Zhu, Lei;Jian, Xingxing;Zhou, Bingjing;Liu, Runqiu;Munoz, Melba;Sun, Wan;Xie, Lu;Chen, Xiang;Peng, Cong;Maurer, Marcus;Li, Jie
慢性自发性荨麻疹（CSU）伴随肠道生态失调，但其相关性仍然难以捉摸。在这里，我们使用宏基因组学测序和短链脂肪酸代谢组学，并评估人类CSU粪便微生物移植，肺炎克雷伯氏菌，罗斯拜瑞氏菌和体内代谢产物的影响。CSU肠道微生物群显示出低多样性和短链脂肪酸生产，但高肠道肺炎克雷伯菌水平与血液短链脂肪酸水平呈负相关，并与高疾病活动性相关。血液脂多糖水平升高，与疾病的快速复发和条件致病菌的高肠道水平有关。CSU微生物组转移和肺炎克雷伯氏菌移植促进IgE介导的肥大细胞（MC）驱动的皮肤炎症反应，并增加受体小鼠的肠道通透性和血液脂多糖积累。人罗斯拜瑞氏菌的移植和己酸盐给药保护受体小鼠免受MC驱动的皮肤炎症。在这里，我们表明CSU中的肠道微生物组改变可能分别减少短链脂肪酸和增加脂多糖水平，并促进MC驱动的皮肤炎症。慢性自发性荨麻疹是一种炎症性皮肤病，与肠道生态失调有关。在这里，作者暗示肠道生态失调与炎症反应的小鼠模型荨麻疹。
Chronic spontaneous urticaria (CSU) comes with gut dysbiosis, but its relevance remains elusive. Here we use metagenomics sequencing and short-chain fatty acids metabolomics and assess the effects of human CSU fecal microbial transplantation, Klebsiella pneumoniae, Roseburia hominis, and metabolites in vivo. CSU gut microbiota displays low diversity and short-chain fatty acids production, but high gut Klebsiella pneumoniae levels, negatively correlates with blood short-chain fatty acids levels and links to high disease activity. Blood lipopolysaccharide levels are elevated, link to rapid disease relapse, and high gut levels of conditional pathogenic bacteria. CSU microbiome transfer and Klebsiella pneumoniae transplantation facilitate IgE-mediated mast cell(MC)-driven skin inflammatory responses and increase intestinal permeability and blood lipopolysaccharide accumulation in recipient mice. Transplantation of Roseburia hominis and caproate administration protect recipient mice from MC-driven skin inflammation. Here, we show gut microbiome alterations, in CSU, may reduce short-chain fatty acids and increase lipopolysaccharide levels, respectively, and facilitate MC-driven skin inflammation. Chronic spontaneous urticarial is an inflammatory skin disease which has been linked to intestinal dysbiosis. Here the authors implicate intestinal dysbiosis with the inflammatory response in a murine model of urticaria.
影响因子：
3.7
作者：
Saluja R;Delin I;Nilsson GP;Adner M
通讯作者：
Adner M