The propionate-GPR41 axis in infancy protects from subsequent bronchial asthma onset

Evidence has accumulated that gut microbiota and its metabolites, in particular the short-chain fatty acid propionate, are significant contributors to the pathogenesis of a variety of diseases. However, little is known regarding its impact on pediatric bronchial asthma, one of the most common allergic diseases in childhood. This study aimed to elucidate whether, and if so how, intestinal propionate during lactation is involved in the development of bronchial asthma. We found that propionate intake through breast milk during the lactation period resulted in a significant reduction of airway inflammation in the offspring in a murine house dust mite-induced asthma model. Moreover, GPR41 was the propionate receptor involved in suppressing this asthmatic phenotype, likely through the upregulation of Toll-like receptors. In translational studies in a human birth cohort, we found that fecal propionate was decreased one month after birth in the group that later developed bronchial asthma. These findings indicate an important role for propionate in regulating immune function to prevent the pathogenesis of bronchial asthma in childhood.

Automated summary

Evidence suggests that gut microbiota and its metabolites, particularly the short-chain fatty acid propionate, play a significant role in the development of various diseases. However, little is known about its impact on pediatric bronchial asthma. This study found that propionate intake through breast milk during lactation reduces airway inflammation and suppresses asthma development through the propionate receptor GPR41 and upregulation of Toll-like receptors. Translational studies in a human birth cohort also showed a decrease in fecal propionate in those who later developed bronchial asthma, highlighting the importance of propionate in immune function regulation.