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Maternal acellular pertussis vaccination in mice impairs cellular immunity to Bordetella pertussis infection in offspring
Violaine Dubois, Jonathan Chatagnon, Manon Depessemier, Camille Locht
Violaine Dubois, Jonathan Chatagnon, Manon Depessemier, Camille Locht
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Research Article Infectious disease Vaccines

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

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Abstract

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.

Authors

Violaine Dubois, Jonathan Chatagnon, Manon Depessemier, Camille Locht

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Figure 3

Effect of maternal aP immunization on recruitment and activation of T cells in lungs and noses.

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Effect of maternal aP immunization on recruitment and activation of T ce...
Neonatal mice born to control (Ctr) or aP-vaccinated mothers (aP) were infected with 5 × 103 CFU B1917 6–7 days after birth and sacrificed 28 dpc. Ten minutes before euthanasia, mice were i.v. injected with anti–CD45-PE (CD45iv) antibody. (A) Representative plots showing the recruitment of CD4+CD45iv– T cells in the lungs (upper plots) and noses (lower plots). (B) Absolute numbers of CD4+CD45iv– T cells in the lungs (left panel) and nose (right panel) of offspring. (C) Representative plots showing the expression of CD11a and CD44 on CD4+ T cells (upper panel) and expression of IL-17 and IFN-γ upon stimulation with PMA and ionomycin (lower panel). (D) Absolute numbers of pulmonary (left) and nasal (right) CD4+ T cells expressing CD44 and CD11a. (E) Percentages of CD4+ T cells producing IL-17 and/or IFN-γ in lungs (left) and noses (right). (F) Absolute numbers of CD44+CD11a+CD4+ T cells expressing IL-17 (left panel), IFN-γ (right panel), or both (middle panel). Results shown are geometric means ± SD. n = 4–5. Mann-Whitney tests were performed to compare Ctr and aP offspring. *P < 0.05; **P < 0.01.

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