Nutrition-induced changes in the microbiota can cause dysbiosis and disease development

Research output: Journal contributionsJournal articlesResearchpeer-review

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Nutrition-induced changes in the microbiota can cause dysbiosis and disease development. / Lachnit, Tim; Ulrich, Laura; Willmer, Fiete M. et al.
In: mBio, Vol. 16, No. 4, e03843-24, 04.2025.

Research output: Journal contributionsJournal articlesResearchpeer-review

Harvard

Lachnit, T, Ulrich, L, Willmer, FM, Hasenbein, T, Steiner, LX, Wolters, M, Herbst, EM & Deines, P 2025, 'Nutrition-induced changes in the microbiota can cause dysbiosis and disease development', mBio, vol. 16, no. 4, e03843-24. https://doi.org/10.1128/mbio.03843-24

APA

Lachnit, T., Ulrich, L., Willmer, F. M., Hasenbein, T., Steiner, L. X., Wolters, M., Herbst, E. M., & Deines, P. (2025). Nutrition-induced changes in the microbiota can cause dysbiosis and disease development. mBio, 16(4), Article e03843-24. https://doi.org/10.1128/mbio.03843-24

Vancouver

Lachnit T, Ulrich L, Willmer FM, Hasenbein T, Steiner LX, Wolters M et al. Nutrition-induced changes in the microbiota can cause dysbiosis and disease development. mBio. 2025 Apr;16(4):e03843-24. doi: 10.1128/mbio.03843-24

Bibtex

@article{c5dc1511984a409a94fbc6a42ae02822,
title = "Nutrition-induced changes in the microbiota can cause dysbiosis and disease development",
abstract = "Eukaryotic organisms are associated with complex microbial communities. Changes within these communities have been implicated in disease development. Nonetheless, it remains unclear whether these changes are a cause or a consequence of disease. Here, we report a causal link between environment-induced shifts in the microbiota and disease development. Using the model organism Hydra, we observed changes in microbial composition when transferring laboratory-grown Hydra to natural lake environments. These shifts were caused not only by new colonizers, through the process of community coalescence (merging of previously separate microbial communities), but also by lake water nutrients. Moreover, selective manipulation of the nutrient environment induced compound-specific shifts in the microbiota followed by disease development. Finally, L-arginine supplementation alone caused a transition in Pseudomonas from symbiotic to pathogenic, leading to an upregulation of immune response genes, tissue degradation, and host death. These findings challenge the notion that the host-associated microbiota is exclusively controlled by the host, highlighting the dynamic interplay between host epithelial environment, microbial colonizer pool, and nutrient conditions of the surrounding water. Furthermore, our results show that overfeeding of the microbiota allows for uncontrolled microbial growth and versatile interactions with the host. Environmental conditions may thus render symbionts a potential hazard to their hosts, blurring the divide between pathogenic and non-pathogenic microbes.",
keywords = "disease, dysbiosis, environment, host-microbe interaction, inflammation, microbiome, microbiota, nutrition, pathogens, Biology",
author = "Tim Lachnit and Laura Ulrich and Willmer, {Fiete M.} and Tim Hasenbein and Steiner, {Leon X.} and Maria Wolters and Herbst, {Eva M.} and Peter Deines",
note = "Publisher Copyright: Copyright {\textcopyright} 2025 Lachnit et al.",
year = "2025",
month = apr,
doi = "10.1128/mbio.03843-24",
language = "English",
volume = "16",
journal = "mBio",
issn = "2161-2129",
publisher = "American Society For Microbiology",
number = "4",

}

RIS

TY - JOUR

T1 - Nutrition-induced changes in the microbiota can cause dysbiosis and disease development

AU - Lachnit, Tim

AU - Ulrich, Laura

AU - Willmer, Fiete M.

AU - Hasenbein, Tim

AU - Steiner, Leon X.

AU - Wolters, Maria

AU - Herbst, Eva M.

AU - Deines, Peter

N1 - Publisher Copyright: Copyright © 2025 Lachnit et al.

PY - 2025/4

Y1 - 2025/4

N2 - Eukaryotic organisms are associated with complex microbial communities. Changes within these communities have been implicated in disease development. Nonetheless, it remains unclear whether these changes are a cause or a consequence of disease. Here, we report a causal link between environment-induced shifts in the microbiota and disease development. Using the model organism Hydra, we observed changes in microbial composition when transferring laboratory-grown Hydra to natural lake environments. These shifts were caused not only by new colonizers, through the process of community coalescence (merging of previously separate microbial communities), but also by lake water nutrients. Moreover, selective manipulation of the nutrient environment induced compound-specific shifts in the microbiota followed by disease development. Finally, L-arginine supplementation alone caused a transition in Pseudomonas from symbiotic to pathogenic, leading to an upregulation of immune response genes, tissue degradation, and host death. These findings challenge the notion that the host-associated microbiota is exclusively controlled by the host, highlighting the dynamic interplay between host epithelial environment, microbial colonizer pool, and nutrient conditions of the surrounding water. Furthermore, our results show that overfeeding of the microbiota allows for uncontrolled microbial growth and versatile interactions with the host. Environmental conditions may thus render symbionts a potential hazard to their hosts, blurring the divide between pathogenic and non-pathogenic microbes.

AB - Eukaryotic organisms are associated with complex microbial communities. Changes within these communities have been implicated in disease development. Nonetheless, it remains unclear whether these changes are a cause or a consequence of disease. Here, we report a causal link between environment-induced shifts in the microbiota and disease development. Using the model organism Hydra, we observed changes in microbial composition when transferring laboratory-grown Hydra to natural lake environments. These shifts were caused not only by new colonizers, through the process of community coalescence (merging of previously separate microbial communities), but also by lake water nutrients. Moreover, selective manipulation of the nutrient environment induced compound-specific shifts in the microbiota followed by disease development. Finally, L-arginine supplementation alone caused a transition in Pseudomonas from symbiotic to pathogenic, leading to an upregulation of immune response genes, tissue degradation, and host death. These findings challenge the notion that the host-associated microbiota is exclusively controlled by the host, highlighting the dynamic interplay between host epithelial environment, microbial colonizer pool, and nutrient conditions of the surrounding water. Furthermore, our results show that overfeeding of the microbiota allows for uncontrolled microbial growth and versatile interactions with the host. Environmental conditions may thus render symbionts a potential hazard to their hosts, blurring the divide between pathogenic and non-pathogenic microbes.

KW - disease

KW - dysbiosis

KW - environment

KW - host-microbe interaction

KW - inflammation

KW - microbiome

KW - microbiota

KW - nutrition

KW - pathogens

KW - Biology

UR - http://www.scopus.com/inward/record.url?scp=105002807647&partnerID=8YFLogxK

U2 - 10.1128/mbio.03843-24

DO - 10.1128/mbio.03843-24

M3 - Journal articles

C2 - 39998180

AN - SCOPUS:105002807647

VL - 16

JO - mBio

JF - mBio

SN - 2161-2129

IS - 4

M1 - e03843-24

ER -

DOI

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