<p>Despite high vaccination coverage, pertussis continues to cause substantial morbidity in infants, largely because acellular pertussis (aP) vaccines do not prevent bacterial carriage and transmission. Whether post-exposure booster vaccination can rapidly reduce respiratory carriage and thereby limit transmission remains unclear. We used an adoptive murine transfer model mimicking waning vaccine-induced antibodies observed in humans to assess the impact of post-exposure aP vaccination following respiratory challenge with <i>Bordetella pertussis</i>. Bacterial loads in the lungs and trachea and pertussis-specific antibody responses were assessed across multiple independent experiments. Post-exposure aP vaccination triggered a rapid recall of pertussis-specific antibodies and significantly accelerated bacterial clearance from both lungs and trachea. Compared with non-boosted immune mice, vaccinated animals showed significantly lower bacterial loads on days 7, 10, and 14 after exposure and cleared <i>Bordetella pertussis</i> earlier (<i>p</i> &lt; 0.01). Similar reductions in bacterial burden were observed with delayed boosting, lower-antigen-content vaccines, and passive immunization. In this preclinical model, post-exposure pertussis booster vaccination efficiently recalls memory B cells and accelerates <i>Bordetella pertussis</i> clearance in the lung and upper airways. These findings support the potential role of post-exposure vaccination strategies as a complementary approach to limit transmission in household and community settings and thus better control epidemics.</p>

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Post-exposure booster vaccination recalls vaccine-induced memory and accelerates Bordetella pertussis clearance in murine lungs and trachea

  • Marie Ballester,
  • Paola Fontannaz,
  • Floriane Auderset,
  • Renato Gualtieri,
  • Paul-Henri Lambert,
  • Claire-Anne Siegrist

摘要

Despite high vaccination coverage, pertussis continues to cause substantial morbidity in infants, largely because acellular pertussis (aP) vaccines do not prevent bacterial carriage and transmission. Whether post-exposure booster vaccination can rapidly reduce respiratory carriage and thereby limit transmission remains unclear. We used an adoptive murine transfer model mimicking waning vaccine-induced antibodies observed in humans to assess the impact of post-exposure aP vaccination following respiratory challenge with Bordetella pertussis. Bacterial loads in the lungs and trachea and pertussis-specific antibody responses were assessed across multiple independent experiments. Post-exposure aP vaccination triggered a rapid recall of pertussis-specific antibodies and significantly accelerated bacterial clearance from both lungs and trachea. Compared with non-boosted immune mice, vaccinated animals showed significantly lower bacterial loads on days 7, 10, and 14 after exposure and cleared Bordetella pertussis earlier (p < 0.01). Similar reductions in bacterial burden were observed with delayed boosting, lower-antigen-content vaccines, and passive immunization. In this preclinical model, post-exposure pertussis booster vaccination efficiently recalls memory B cells and accelerates Bordetella pertussis clearance in the lung and upper airways. These findings support the potential role of post-exposure vaccination strategies as a complementary approach to limit transmission in household and community settings and thus better control epidemics.