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Open AccessArticle
From Compensation to Collapse: UVB-Driven Disruption of Host–Microbiota Homeostasis Exacerbates Amphibian Ecological Risk
by
Zi’ao Yuan
Zi’ao Yuan
,
Jirui Fei
Jirui Fei ,
Siqi Li
Siqi Li ,
Yueluan Wu
Yueluan Wu and
Peng Liu
Peng Liu *
College of Life Science and Technology, Harbin Normal University, Harbin 150080, China
*
Author to whom correspondence should be addressed.
Submission received: 9 October 2025
/
Revised: 29 October 2025
/
Accepted: 5 November 2025
/
Published: 7 November 2025
Simple Summary
Amphibians face severe threats from increasing ultraviolet-B (UVB) radiation due to ozone depletion and climate change. Using Xenopus laevis as a model, this study investigated the effects of varying UVB doses on multi-organ health and symbiotic microbiota. We found that low-dose UVB activated protective responses, including elevated antioxidant enzyme activities and proliferation of anti-inflammatory bacteria. However, beyond a specific threshold, UVB exposure induced a collapse of the redox defense system, damaged skin and gut barriers, and led to microbial dysbiosis. Collectively, these changes exacerbated physiological stress and compromised the host’s ecological adaptability. Our study reveals a cross-organ mechanism through which UVB disrupts host–microbe homeostasis, thereby threatening amphibian survival. These findings provide a scientific basis for predicting population decline risks under ongoing climate change and offer insights for developing targeted conservation strategies, such as habitat shade management and microbiota intervention.
Abstract
The synergistic effects of stratospheric ozone depletion and climate change are intensifying surface ultraviolet-B (UVB) radiation, posing a severe threat to amphibians—one of the most endangered vertebrate groups globally. Xenopus laevis, with its cutaneous respiration and limited photoprotective mechanisms, exhibits high sensitivity to UVB, making it a suitable model for ecotoxicological studies. While UVB is known to cause DNA damage, immune suppression, and microbial dysbiosis, its mechanisms in multi-organ interactions, dose–response thresholds, and host–microbiome regulatory networks remain poorly understood. This study employed a gradient UVB exposure regime integrated with histopathology, oxidative stress assays, and 16S rRNA sequencing to systematically evaluate the effects of UVB on (1) cascade damage across skin, liver, and intestinal barriers; (2) immune cell distribution; (3) redox dynamics; and (4) microbial community structure and function. Our findings demonstrate that low-dose UVB activated compensatory antioxidant defenses without structural disruption, whereas exposure beyond a critical threshold induced nonlinear redox collapse, microbial dysbiosis, and multi-organ barrier failure, collectively exacerbating ecological adaptation risks. These results reveal a cross-scale mechanism by which UVB impairs amphibian health via disruption of host–microbe homeostasis, providing a conceptual and empirical framework for assessing species vulnerability under ongoing climate change.
Share and Cite
MDPI and ACS Style
Yuan, Z.; Fei, J.; Li, S.; Wu, Y.; Liu, P.
From Compensation to Collapse: UVB-Driven Disruption of Host–Microbiota Homeostasis Exacerbates Amphibian Ecological Risk. Animals 2025, 15, 3236.
https://doi.org/10.3390/ani15223236
AMA Style
Yuan Z, Fei J, Li S, Wu Y, Liu P.
From Compensation to Collapse: UVB-Driven Disruption of Host–Microbiota Homeostasis Exacerbates Amphibian Ecological Risk. Animals. 2025; 15(22):3236.
https://doi.org/10.3390/ani15223236
Chicago/Turabian Style
Yuan, Zi’ao, Jirui Fei, Siqi Li, Yueluan Wu, and Peng Liu.
2025. "From Compensation to Collapse: UVB-Driven Disruption of Host–Microbiota Homeostasis Exacerbates Amphibian Ecological Risk" Animals 15, no. 22: 3236.
https://doi.org/10.3390/ani15223236
APA Style
Yuan, Z., Fei, J., Li, S., Wu, Y., & Liu, P.
(2025). From Compensation to Collapse: UVB-Driven Disruption of Host–Microbiota Homeostasis Exacerbates Amphibian Ecological Risk. Animals, 15(22), 3236.
https://doi.org/10.3390/ani15223236
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