The use of antibiotics in early life increases the risk of developing allergy and asthma in childhood. Although microbial dysbiosis and levels of certain microbial metabolites have been linked to this increased risk, the underlying mechanisms are poorly understood. Marsland and colleagues now show that antibiotic-induced depletion of the gut microbiome in early life reduces systemic levels of the metabolite indole-3-propionic acid (IPA). Although transient in nature, this causes long-lasting mitochondrial damage to lung epithelial cells.

At steady state (40 days of cohousing), EL-Abx mice showed no overt changes in immune cell number or composition, or in gut permeability. However, stimulation of lung structural cells in culture with HDM or lipopolysaccharide induced higher levels of various chemokines from EL-Abx mice than non-treated mice.