Antibiotics drive immunometabolic rewiring of human immune responses

Ciprofloxacin alters mitochondrial gene expression in primary human immune cells, driving lineage-specific immune responses and heightened sensitivity of T-cells, including impaired expansion and activation.

• Why it matters: Antibiotics are assessed mainly for antimicrobial activity and microbiome disruption, but their direct effects on host immunometabolic activation—especially via mitochondria—remain insufficiently mapped.
• What they did: The study comprehensively analyzed clinically used antibiotics on activation of primary human immune cells, then mechanistically focused on ciprofloxacin’s mitochondrial gene expression, function, and metabolism, including tests with inactivated bacteria and live viral infection.
• The result: In mice, immune activation is altered shortly after a single dose of antibiotic administration, supporting mitochondrial perturbation as a mechanism that can reshape host-pathogen interactions during antimicrobial therapy.

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