A single early-in-life antibiotic course increases susceptibility to DSS-induced colitis.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model (murine study with no human data).
PubMed 32711559 · doi:10.1186/s13073-020-00764-z
What was done
Mice were given an early-life pulsed antibiotic treatment (PAT) using either tylosin (a macrolide) or amoxicillin (a beta-lactam) and subsequently challenged with dextran sodium sulfate (DSS) to induce colitis. Researchers analyzed the gut microbiota using 16S rRNA gene sequencing and intestinal T cells via flow cytometry. To assess whether the altered microbiome directly mediated disease susceptibility, antibiotic-perturbed or control microbiota collected 40 days post-treatment were transferred into germ-free mouse pups prior to DSS challenge.
What was found
A single early-in-life course of antibiotics worsened subsequent DSS-induced colitis severity, altered the microbial community, and modified mucosal immune cell composition. Transferring the antibiotic-perturbed microbiota to germ-free mice transferred the heightened susceptibility to DSS colitis, demonstrating a direct, durable effect of the altered microbiome. The abstract reports no quantitative values or effect sizes.
Why it matters
This study provides mechanistic preclinical evidence supporting epidemiological observations that early-childhood antibiotic exposure can disrupt long-term microbiome-immune development and increase susceptibility to inflammatory bowel diseases.
Limits
The study was conducted entirely in mice using a chemically induced (DSS) colitis model, which does not capture the full complexity of human inflammatory bowel disease. Specific sample sizes, effect sizes, statistical parameters, and comparative differences between tylosin and amoxicillin are omitted from the abstract.
Cited by
- supports Early-life microbiome disruption or depletion increases susceptibility to developing inflammatory bowel disease (IBD) later in life.