Poor association between 13-valent pneumococcal conjugate vaccine-induced serum and mucosal antibody responses with experimental Streptococcus pneumoniae serotype 6B colonisation.

Carriage Colonisation PCV Pneumococcal conjugate vaccine Pneumococcus anti-CPS

Journal

Vaccine
ISSN: 1873-2518
Titre abrégé: Vaccine
Pays: Netherlands
ID NLM: 8406899

Informations de publication

Date de publication:
02 Apr 2024
Historique:
received: 10 11 2023
revised: 23 02 2024
accepted: 21 03 2024
medline: 4 4 2024
pubmed: 4 4 2024
entrez: 3 4 2024
Statut: aheadofprint

Résumé

Pneumococcal carriage is the primary reservoir for transmissionand a prerequisite for invasive pneumococcal disease. Pneumococcal Conjugate Vaccine 13 (PCV13) showed a 62% efficacy in protection against experimental Streptococcus pneumoniae serotype 6B (Spn6B) carriage in a controlled human infection model (CHIM) of healthy Malawian adults. We, therefore, measured humoral responses to experimental challenge and PCV-13 vaccination and determined the association with protection against pneumococcal carriage. We vaccinated 204 young, healthy Malawian adults with PCV13 or placebo and nasally inoculated them with Spn6B at least four weeks post-vaccination to establish carriage. We collected peripheral blood and nasal lining fluid at baseline, 4 weeks post-vaccination (7 days pre-inoculation), 2, 7, 14 and > 1 year post-inoculation. We measured the concentration of anti-serotype 6B Capsular Polysaccharide (CPS) Immunoglobulin G (IgG) and IgA antibodies in serum and nasal lining fluid using the World Health Organization (WHO) standardised enzyme-linked immunosorbent assay (ELISA). PCV13-vaccinated adults had higher serum IgG and nasal IgG/IgA anti-Spn6B CPS-specific binding antibodies than placebo recipients 4 to 6 weeks post-vaccination, which persisted for at least a year after vaccination. Nasal challenge with Spn6B did not significantly alter serum or nasal anti-CPS IgG binding antibody titers with or without experimental pneumococcal carriage. Pre-challenge titers of PCV13-induced serum IgG and nasal IgG/IgA anti-Spn6B CPS binding antibodies did not significantly differ between those that got experimentally colonised by Spn6B compared to those that did not. This study demonstrates that despite high PCV13 efficacy against experimental Spn6B carriage in young, healthy Malawian adults, robust vaccine-induced systemic and mucosal anti-Spn6B CPS binding antibodies did not directly relate to protection.

Sections du résumé

BACKGROUND BACKGROUND
Pneumococcal carriage is the primary reservoir for transmissionand a prerequisite for invasive pneumococcal disease. Pneumococcal Conjugate Vaccine 13 (PCV13) showed a 62% efficacy in protection against experimental Streptococcus pneumoniae serotype 6B (Spn6B) carriage in a controlled human infection model (CHIM) of healthy Malawian adults. We, therefore, measured humoral responses to experimental challenge and PCV-13 vaccination and determined the association with protection against pneumococcal carriage.
METHODS METHODS
We vaccinated 204 young, healthy Malawian adults with PCV13 or placebo and nasally inoculated them with Spn6B at least four weeks post-vaccination to establish carriage. We collected peripheral blood and nasal lining fluid at baseline, 4 weeks post-vaccination (7 days pre-inoculation), 2, 7, 14 and > 1 year post-inoculation. We measured the concentration of anti-serotype 6B Capsular Polysaccharide (CPS) Immunoglobulin G (IgG) and IgA antibodies in serum and nasal lining fluid using the World Health Organization (WHO) standardised enzyme-linked immunosorbent assay (ELISA).
RESULTS RESULTS
PCV13-vaccinated adults had higher serum IgG and nasal IgG/IgA anti-Spn6B CPS-specific binding antibodies than placebo recipients 4 to 6 weeks post-vaccination, which persisted for at least a year after vaccination. Nasal challenge with Spn6B did not significantly alter serum or nasal anti-CPS IgG binding antibody titers with or without experimental pneumococcal carriage. Pre-challenge titers of PCV13-induced serum IgG and nasal IgG/IgA anti-Spn6B CPS binding antibodies did not significantly differ between those that got experimentally colonised by Spn6B compared to those that did not.
CONCLUSION CONCLUSIONS
This study demonstrates that despite high PCV13 efficacy against experimental Spn6B carriage in young, healthy Malawian adults, robust vaccine-induced systemic and mucosal anti-Spn6B CPS binding antibodies did not directly relate to protection.

Identifiants

pubmed: 38570270
pii: S0264-410X(24)00360-8
doi: 10.1016/j.vaccine.2024.03.055
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

G Tembo (G)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi. Electronic address: gtembo@mlw.mw.

M Mayuni (M)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

R Kamng'ona (R)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

L Chimgoneko (L)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

G Chiwala (G)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

S Sichone (S)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

B Galafa (B)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

F Thole (F)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

C Mkandawire (C)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

A E Chirwa (AE)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

E Nsomba (E)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

V Nkhoma (V)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

C Ngoliwa (C)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

N Toto (N)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

L Makhaza (L)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

A Muyaya (A)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

E Kudowa (E)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

M Y R Henrion (MYR)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi; Liverpool School of Tropical Medicine, Clinical Sciences Department, Pembroke Place, Liverpool, UK.

D Dula (D)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

B Morton (B)

Liverpool School of Tropical Medicine, Clinical Sciences Department, Pembroke Place, Liverpool, UK.

T Chikaonda (T)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi.

S B Gordon (SB)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi; Liverpool School of Tropical Medicine, Clinical Sciences Department, Pembroke Place, Liverpool, UK.

K C Jambo (KC)

Malawi-Liverpool-Wellcome Research Programme, Blantyre, Malawi; Liverpool School of Tropical Medicine, Clinical Sciences Department, Pembroke Place, Liverpool, UK. Electronic address: kjambo@mlw.mw.

Classifications MeSH