Antibiotics May Harm Infant Immunity, Study Finds Potential Reversal

Key Molecule Inosine Shows Promise in Restoring Immune Defenses

New research suggests early-life antibiotic exposure can significantly impact a baby’s developing immune system, potentially leaving them vulnerable to respiratory infections. Scientists have identified a naturally occurring metabolite, inosine, that may offer a way to mend this damage.

Disrupting Immune Signals

A University of Rochester Medical Center (URMC) study, published in the journal *Cell*, discovered that antibiotics given during pregnancy and infancy can weaken the immune system’s ability to fight off illnesses like the flu. Researchers observed that these drugs disrupt the gut microbiome’s production of inosine, a crucial molecule for immune cell maturation.

“Think of inosine as a molecular messenger. It travels from the gut to developing immune cells, telling them how to mature properly and prepare for future infections.”

—Hitesh Deshmukh, MD, PhD, Senior Author and Chief of Neonatology at UR Medicine Golisano Children’s Hospital

This disruption affects the formation of tissue-resident memory T cells, specialized immune cells that reside in the lungs and offer long-term protection against viral threats. The study’s findings are part of a larger NIH initiative examining how early-life exposures influence lifelong disease risks.

Restoring Immune Function in Mice

The research team found that supplementing inosine in mice exposed to antibiotics helped correct the immune system deficiencies. This breakthrough opens avenues for developing therapies to strengthen immune memory in infants at risk.

Insights from Human and Animal Models

The study utilized both mouse models and human infant lung tissue. Researchers compared infant mice given common antibiotics (ampicillin, gentamicin, and vancomycin) with those with natural gut bacteria. The antibiotic-exposed mice showed fewer protective CD8+ T cells in their lungs and impaired ability to form memory cells.

These immune deficits persisted into adulthood, indicating potentially permanent changes in immune development. Crucially, the team analyzed lung samples from human infants in an NIH-funded biobank, confirming similar immune deficits in those exposed to antibiotics.

Dr. Gloria Pryhuber, a neonatologist at GCH, was instrumental in the research, providing access to her BRINDL biobank of infant lung samples collected over 15 years through NIH funding. This biobank enabled the team to validate their findings in human cells.

Dr. Deshmukh stated, “We’ve discovered that the gut microbiome acts as a teacher for the developing immune system. When antibiotics disrupt this natural education process, it’s like removing key chapters from a textbook: the immune system never learns crucial lessons about fighting respiratory infections.”

The study’s results could guide future research into interventions like dietary supplements or metabolite therapies aimed at bolstering newborn immunity without solely relying on antibiotics or potentially risky probiotics. A 2023 report noted that antibiotic resistance is a growing global health threat, underscoring the need for careful antibiotic stewardship, especially in vulnerable populations (WHO).

Future Therapeutic Possibilities

“This suggests we might be able to protect at-risk infants through targeted supplementation,” Dr. Deshmukh added. “While much more research is needed before this approach could be applied clinically, it gives us a path forward.”