Nutrition-induced changes in the microbiota can cause dysbiosis and disease development
Publikation: Beiträge in Zeitschriften › Zeitschriftenaufsätze › Forschung › begutachtet
Standard
in: mBio, Jahrgang 16, Nr. 4, e03843-24, 04.2025.
Publikation: Beiträge in Zeitschriften › Zeitschriftenaufsätze › Forschung › begutachtet
Harvard
APA
Vancouver
Bibtex
}
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 -