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尼罗罗非鱼肠道微生物群对水温升高的变化及恢复力伴随着免疫功能的恢复。

Alterations and resilience of intestinal microbiota to increased water temperature are accompanied by the recovery of immune function in Nile tilapia.

作者信息

Wu Zhenbing, Zhang Qianqian, Wang Xiehao, Li Aihua

机构信息

State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, 430072, China.

School of Environmental Science and Engineering, Huazhong University of Science and Technology, Wuhan, 430074, China.

出版信息

Sci Rep. 2025 Feb 11;15(1):5094. doi: 10.1038/s41598-025-87980-y.

DOI:10.1038/s41598-025-87980-y
PMID:39934152
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11814331/
Abstract

In the context of ongoing global warming, fish, as aquatic ectotherms, are highly vulnerable to increased water temperature caused by climate change and extreme heatwaves because of their inability to maintain their body temperature. After prolonged coevolution, the intestinal microbiota has become an integral part of fish and plays a pivotal role in immunity and metabolism. To date, however, little is known about the effects of increased water temperature on the intestinal microbiota of fish, particularly the intestinal mucosa-associated microbiota. Here, we investigated the variation patterns of the intestinal microbiota and immune status in Nile tilapia (Oreochromis niloticus; 125.02 ± 4.55 g) under increased water temperature. The results showed that the microbial diversity, structure, dominant microbes, and predicted function of fish intestinal microbiota were resilient to low-level warming (increasing by 2 °C) but not to high-level warming (increasing by 8 °C) and that fish immune parameters (serum lysozyme content and bactericidal activity) recovered simultaneously. Notably, along with compromised immune function, short-term warming (7 days) drove a significant increase in the microbial richness and diversity of fish intestinal mucosae, in which the overgrowth of opportunistic pathogens such as Romboutsia ilealis, Escherichia-Shigella, Fusobacterium, Streptococcus, Acinetobacter, and Enterobacter inhibited the colonization of potential probiotics such as Cetobacterium, ultimately resulting in a significant reduction in metabolic pathways and a significant increase in the potentially pathogenic phenotype. After long-term warming (37 days), the above alterations disappeared in low-level warming but remained in high-level warming. Critically, long-term warming disrupted the network complexity and stability of the intestinal mucosa- and digesta-associated microbiota to different extents. Collectively, this study revealed that the alterations and resilience of intestinal microbiota to increased water temperature coincided with the recovery of immune function in fish. Our findings extend the understanding of how the intestinal microbiota in aquatic ectotherms respond to increased water temperature, providing important implications for harnessing the potential benefits of host-associated microorganisms to enhance their resilience to climate change.

摘要

在全球持续变暖的背景下,鱼类作为水生变温动物,由于无法维持体温,极易受到气候变化和极端热浪导致的水温升高的影响。经过长期的共同进化,肠道微生物群已成为鱼类不可或缺的一部分,并在免疫和代谢中发挥关键作用。然而,迄今为止,关于水温升高对鱼类肠道微生物群,尤其是肠道黏膜相关微生物群的影响知之甚少。在此,我们研究了尼罗罗非鱼(Oreochromis niloticus;125.02±4.55克)在水温升高情况下肠道微生物群和免疫状态的变化模式。结果表明,鱼类肠道微生物群的微生物多样性、结构、优势微生物和预测功能对低水平升温(升高2°C)具有弹性,但对高水平升温(升高8°C)不具有弹性,并且鱼类免疫参数(血清溶菌酶含量和杀菌活性)同时恢复。值得注意的是,随着免疫功能受损,短期升温(7天)促使鱼类肠道黏膜的微生物丰富度和多样性显著增加,其中诸如回肠罗氏菌、埃希氏-志贺氏菌属、梭杆菌属、链球菌属、不动杆菌属和肠杆菌属等机会致病菌的过度生长抑制了诸如鲸杆菌属等潜在益生菌的定殖,最终导致代谢途径显著减少和潜在致病表型显著增加。长期升温(37天)后,上述变化在低水平升温中消失,但在高水平升温中依然存在。至关重要的是,长期升温在不同程度上破坏了肠道黏膜和消化物相关微生物群的网络复杂性和稳定性。总体而言,本研究表明肠道微生物群对水温升高的变化和弹性与鱼类免疫功能的恢复相一致。我们的研究结果扩展了对水生变温动物肠道微生物群如何应对水温升高的理解,为利用宿主相关微生物的潜在益处以增强其对气候变化的适应力提供了重要启示。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/0494f394465d/41598_2025_87980_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/f61daa0678b4/41598_2025_87980_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/1cb872c1eb79/41598_2025_87980_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/0494f394465d/41598_2025_87980_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/f61daa0678b4/41598_2025_87980_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/f6e7527f7d6e/41598_2025_87980_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/d7ab7614a67c/41598_2025_87980_Fig3_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/1cb872c1eb79/41598_2025_87980_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ef/11814331/0494f394465d/41598_2025_87980_Fig6_HTML.jpg

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