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Growth promotion and antibiotic induced metabolic shifts in the chicken gut microbiome
Antimicrobial growth promoters (AGP) have played a decisive role in animal agriculture for over half a century. Despite mounting concerns about antimicrobial resistance and demand for antibiotic alternatives, a thorough understanding of how these compounds drive performance is missing. Here we inves...
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Published in: | Communications biology 2022-04, Vol.5 (1), p.293-293, Article 293 |
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Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Antimicrobial growth promoters (AGP) have played a decisive role in animal agriculture for over half a century. Despite mounting concerns about antimicrobial resistance and demand for antibiotic alternatives, a thorough understanding of how these compounds drive performance is missing. Here we investigate the functional footprint of microbial communities in the cecum of chickens fed four distinct AGP. We find relatively few taxa, metabolic or antimicrobial resistance genes similarly altered across treatments, with those changes often driven by the abundances of core microbiome members. Constraints-based modeling of 25 core bacterial genera associated increased performance with fewer metabolite demands for microbial growth, pointing to altered nitrogen utilization as a potential mechanism of narasin, the AGP with the largest performance increase in our study. Untargeted metabolomics of narasin treated birds aligned with model predictions, suggesting that the core cecum microbiome might be targeted for enhanced performance via its contribution to host-microbiota metabolic crosstalk.
This study compares the functional profiles of the cecal microbiome among chickens fed four different antimicrobial growth promoters. Chickens receiving narasin exhibited the largest performance increase via apparent nitrogen recycling by the core cecal microbiome. |
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ISSN: | 2399-3642 2399-3642 |
DOI: | 10.1038/s42003-022-03239-6 |