The Alteration of Akkermansiaceae/Lachnospiraceae Ratio Is a Microbial Feature of Antibiotic-Induced Microbiota Remodeling

Abstract

Antibiotic treatment has been shown to cause gut microbiota dysbiosis. However, lacking critical features defining gut microbiota dysbiosis makes it challenging to prevent. By co-occurrence network analysis, we found that despite short antibiotic courses eliminating certain microbial taxa, the Akkermansia genus played the role of a high-centrality hub to maintain microbiota homeostasis. When the antibiotic courses continued, the elimination of Akkermansia induced a significant microbiota remodeling of the gut microbiota networks. Based on this finding, we found that under long-term antibiotic stress, the gut microbiota was rearranged into a stable network with a significantly lower Akkermansiaceae/ Lachnospiraceae (A/L) ratio and no microbial hub. By functional prediction analysis, we confirmed that the gut microbiota with a low A/L ratio also had enhanced mobile elements and biofilm-formation functions that may be associated with antibiotic resistance. This study identified A/L ratio as an indicator of antibiotic-induced dysbiosis. This work reveals that besides the abundance of specific probiotics, the hierarchical structure also critically impacts the microbiome function. Co-occurrence analysis may help better monitor the microbiome dynamics than only comparing the differentially abundant bacteria between samples.

Intestinal dual-specificity phosphatase 6 regulates the cold-induced gut microbiota remodeling to promote white adipose browning

“…However, it is still unclear whether the dynamics of A. muciniphila abundance contribute to the physiological rearrangement of the gut microbiota. Interestingly, specific rearrangement between Akkermansiaceae and Lachnospiraceae has been observed in patients receiving prolonged antibiotic treatment, suggesting a potential role of A. muciniphila in mediating these changes 50 . The downregulation of A. muciniphila abundance is a well-known cold-adapted phenotype in mice 19 .…”