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维生素 D 影响斑马鱼的肠道微生物群和乙酸盐产生,以促进肠道免疫抵抗入侵病原体。

Vitamin D influences gut microbiota and acetate production in zebrafish () to promote intestinal immunity against invading pathogens.

机构信息

Key Laboratory of Aquaculture Nutrition and Feed, Ministry of Agriculture & Key Laboratory of Mariculture, Ministry of Education, College of Fisheries, Ocean University of China, Qingdao, China.

State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.

出版信息

Gut Microbes. 2023 Jan-Dec;15(1):2187575. doi: 10.1080/19490976.2023.2187575.

DOI:10.1080/19490976.2023.2187575
PMID:36879441
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10012952/
Abstract

Although evidence has shown that vitamin D (VD) influences gut homeostasis, limited knowledge is available how VD regulates intestinal immunity against bacterial infection. In the present study, mutant zebrafish, lacking the capacity to metabolize VD, and zebrafish fed a diet devoid of VD, were utilized as VD-deficient animal models. Our results confirmed that the expression of antimicrobial peptides (AMPs) and IL-22 was restrained and the susceptibility to bacterial infection was increased in VD-deficient zebrafish. Furthermore, VD induced AMP expression in zebrafish intestine by activating IL-22 signaling, which was dependent on the microbiota. Further analysis uncovered that the abundance of the acetate-producer in VD-deficient zebrafish was reduced compared to WT fish. Unexpectedly, VD promoted the growth and acetate production of under culture . Importantly, acetate treatment rescued the suppressed expression of β-defensins in VD-deficient zebrafish. Finally, neutrophils contributed to VD-induced AMP expression in zebrafish. In conclusion, our study elucidated that VD modulated gut microbiota composition and production of short-chain fatty acids (SCFAs) in zebrafish intestine, leading to enhanced immunity.

摘要

虽然有证据表明维生素 D(VD)会影响肠道内稳态,但对于 VD 如何调节肠道免疫以抵抗细菌感染的知识有限。在本研究中,我们利用缺乏代谢 VD 能力的突变型斑马鱼和缺乏 VD 的饮食喂养的斑马鱼作为 VD 缺乏的动物模型。我们的研究结果证实,缺乏 VD 的斑马鱼的抗菌肽(AMP)和 IL-22 的表达受到抑制,对细菌感染的易感性增加。此外,VD 通过激活 IL-22 信号通路诱导斑马鱼肠道中 AMP 的表达,这依赖于微生物群。进一步的分析揭示,与 WT 鱼相比,缺乏 VD 的斑马鱼中乙酸产生菌的丰度降低。出乎意料的是,VD 在培养物中促进了 的生长和乙酸的产生。重要的是,乙酸处理可挽救缺乏 VD 的斑马鱼中 β-防御素表达的抑制。最后,中性粒细胞有助于 VD 诱导的斑马鱼 AMP 表达。总之,我们的研究阐明了 VD 调节了斑马鱼肠道中的肠道微生物群落组成和短链脂肪酸(SCFA)的产生,从而增强了免疫力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/04cd365e8a8a/KGMI_A_2187575_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/0b4058cff974/KGMI_A_2187575_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/ab47e6c5a6c8/KGMI_A_2187575_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/fb0cdc4cc4c7/KGMI_A_2187575_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/880dd3b81fae/KGMI_A_2187575_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/842a598c3604/KGMI_A_2187575_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/04cd365e8a8a/KGMI_A_2187575_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/0b4058cff974/KGMI_A_2187575_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/ab47e6c5a6c8/KGMI_A_2187575_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/fb0cdc4cc4c7/KGMI_A_2187575_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/880dd3b81fae/KGMI_A_2187575_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/842a598c3604/KGMI_A_2187575_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0eee/10012952/04cd365e8a8a/KGMI_A_2187575_F0006_OC.jpg

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