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Mucosal Immunol. 2018 Nov;11(6):1753-1762. doi: 10.1038/s41385-018-0073-9. Epub 2018 Aug 16.

IL-17-dependent SIgA-mediated protection against nasal Bordetella pertussis infection by live attenuated BPZE1 vaccine.

Solans L1,2,3,4, Debrie AS5,6,7,8, Borkner L9, Aguiló N10,11, Thiriard A5,6,7,8, Coutte L5,6,7,8, Uranga S10,11, Trottein F5,6,7,8, Martín C10,11, Mills KHG9, Locht C5,6,7,8.

Author information

Center of Infection and Immunity of Lille, Institut Pasteur de Lille, 59019, Lille, France.
Inserm U1019, 59019, Lille, France.
CNRS UMR8204, 59019, Lille, France.
Univ. Lille, 59019, Lille, France.
Center of Infection and Immunity of Lille, Institut Pasteur de Lille, 59019, Lille, France.
Inserm U1019, 59019, Lille, France.
CNRS UMR8204, 59019, Lille, France.
Univ. Lille, 59019, Lille, France.
Immune Regulation Research Group, School of Biochemistry and Immunology, Trinity College Dublin, Trinity Biomedical Science Institute, Dublin 2, Ireland.
Grupo de Genética de Micobacterias, Dpto. de Microbiología, Medicina Preventiva y Salud Pública, C/Domingo Miral s/n, 50009, Zaragoza, Spain.
CIBER Enfermedades Respiratorias, Instituto de Salud Carlos III, 28029, Madrid, Spain.


BPZE1 is a live attenuated Bordetella pertussis vaccine for nasal administration to mimic the natural route of infection. Here, we studied the mechanism of BPZE1-induced immunity in the murine nasal cavity in contrast to acellular vaccine (aPV), although both vaccines protected against lung colonization. Transfer of splenocytes or serum from BPZE1-vaccinated or aPV-vaccinated mice protected naïve mice against lung colonization but not against nasal colonization. However, transfer of nasal washes from BPZE1-vaccinated mice resulted in protection against nasal colonization, which was lost in IgA-deficient or poly-Ig receptor-deficient mice, indicating that it depends on secretory IgA (SIgA) induction induced in the nose. BPZE1-induced protection against nasal colonization was long-lived despite the relatively rapid decay of SIgA, indicating a potent BPZE1-induced local memory response, likely due to CD4+ tissue-resident memory T cells induced in the nose by BPZE1. These cells produced interleukin-17 (IL-17), known to be important for SIgA secretion. Furthermore, BPZE1 failed to protect Il17-/- mice against nasal colonization by B. pertussis and induced only background levels of nasal SIgA. Thus, our results show important differences in the protective mechanism between the upper and the lower murine respiratory tract and demonstrate an IL-17-dependent SIgA-mediated mechanism of BPZE1-induced protection against B. pertussis nasopharyngeal colonization.

[Indexed for MEDLINE]

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