Abstract
BackgroundThe magnitude of microbiota perturbations after exposure to antibiotics varies among individuals. It has been suggested that the composition of pre-treatment microbiota underpins personalized responses to antibiotics. However, this hypothesis has not been directly tested in humans. In this high-throughput amplicon study, we analyzed 16S ribosomal RNA gene sequences of 260 stool samples collected twice weekly from 39 patients with acute leukemia during their ~ 4 weeks of hospitalization for chemotherapy while they received multiple antibiotics.ResultsDespite heavy and sustained antibiotic pressure, microbial communities in samples from the same patient remained more similar to one another than to those from other patients. Principal component mixed effect regression using microbiota and granular antibiotic exposure data showed that microbiota departures from baseline depend on the composition of the pre-treatment microbiota. Penalized generalized estimating equations identified 6 taxa within pre-treatment microbiota that predicted the extent of antibiotic-induced perturbations.ConclusionsOur results indicate that specific species in pre-treatment microbiota determine personalized microbiota responses to antibiotics in humans. Thus, precision interventions targeting pre-treatment microbiota may prevent antibiotic-induced dysbiosis and its adverse clinical consequences.ABphCC6GsQLEC5Cqxkd6FXVideo abstract
Highlights
The magnitude of microbiota perturbations after exposure to antibiotics varies among individuals
We studied patients with acute myeloid leukemia (AML) receiving inpatient chemotherapy, a prototype setting for heavy sustained antibiotic exposure
These findings offer a mechanistic explanation for individualized responses to antibiotics and introduce novel targets for precision interventions to prevent antibiotic-induced dysbiosis and its adverse clinical consequences
Summary
The magnitude of microbiota perturbations after exposure to antibiotics varies among individuals. It has been suggested that the composition of pre-treatment microbiota underpins personalized responses to antibiotics. This hypothesis has not been directly tested in humans. We hypothesize that pre-treatment microbiota in humans is a determinant of community resistance as measured inversely by the magnitude of microbiota deviation from baseline during phase 1. Germ-free mice humanized with fecal microbiota from different donors show different microbiota responses to the same antibiotic [16], suggesting that pre-treatment microbiota may underpin individualized responses. It is unknown whether and to what extent specific species in baseline microbiota modulate community resistance against antibiotic perturbation
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