Maternal acellular pertussis vaccination in mice impairs cellular immunity to Bordetella pertussis infection in offspring.

Given the resurgence of pertussis, several countries have introduced maternal tetanus, diphtheria, and acellular pertussis (aP) vaccination during pregnancy to protect young infants against severe pertussis. Although protective against the disease, the effect of maternal aP vaccination on bacterial colonization of the offspring is unknown. Here, we used a mouse model to demonstrate that maternal aP immunization, either before or during pregnancy, protects pups from lung colonization by Bordetella pertussis. However, maternal aP vaccination resulted in significantly prolonged nasal carriage of B. pertussis by inhibiting the natural recruitment of IL-17-producing resident memory T cells and ensuing neutrophil influx in the nasal tissue, especially of those with proinflammatory and cytotoxic properties. Prolonged nasal carriage after aP vaccination is due to IL-4 signaling, as prolonged nasal carriage is abolished in IL-4Rα-/- mice. The effect of maternal aP vaccination can be transferred transplacentally to the offspring or via breastfeeding and is long-lasting, as it persists into adulthood. Maternal aP vaccination may, thus, augment the B. pertussis reservoir.