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Intestinal commensal bacteria mediate lung mucosal immunity and promote resistance of newborn mice to infection

Postnatal colonization by intestinal commensal bacteria directs migration of innate lymphoid cells to the lungs and promotes resistance of newborn mice to pneumonia. Gut microbiota: A driving force in lung mucosal defense Interactions between the host immune system and intestinal commensal bacteria shape immune system development. Gray et al. now report that host-commensal interactions extend beyond the local environment and shape the repertoires of immune cells at extraintestinal sites such as the lungs. Exposure to commensals in the developmental window of the newborn period directed lung-selective trafficking of group 3 innate lymphoid cells (ILC3), a group of sentinel cells that maintain mucosal homeostasis. This was mediated by intestinal dendritic cells, which induced expression of the lung homing signal CCR4 on the ILC3. Lung-selective trafficking of ILC3 promoted the resistance of newborn mice to pneumonia. These data explain the association between widespread use of antibiotics and an increased risk of pneumonia in newborn infants. Immature mucosal defenses contribute to increased susceptibility of newborn infants to pathogens. Sparse knowledge of age-dependent changes in mucosal immunity has hampered improvements in neonatal morbidity because of infections. We report that exposure of neonatal mice to commensal bacteria immediately after birth is required for a robust host defense against bacterial pneumonia, the leading cause of death in newborn infants. This crucial window was characterized by an abrupt influx of interleukin-22 (IL-22)–producing group 3 innate lymphoid cells (IL-22+ILC3) into the lungs of newborn mice. This influx was dependent on sensing of commensal bacteria by intestinal mucosal dendritic cells. Disruption of postnatal commensal colonization or selective depletion of dendritic cells interrupted the migratory program of lung IL-22+ILC3 and made the newborn mice more susceptible to pneumonia, which was reversed by transfer of commensal bacteria after birth. Thus, the resistance of newborn mice to pneumonia relied on commensal bacteria–directed ILC3 influx into the lungs, which mediated IL-22–dependent host resistance to pneumonia during this developmental window. These data establish that postnatal colonization by intestinal commensal bacteria is pivotal in the development of the lung defenses of newborns.