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Exacerbated lung inflammation in offspring with high maternal antibody levels following secondary RSV exposure

Jinhua Ma1, Ting Gong1, Tingting Luo1

  • 1Department of Respiratory Medicine Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing, China.

Frontiers in Immunology
|May 15, 2024
PubMed

Insights

Maternal vaccination against respiratory syncytial virus (RSV) protects newborns initially but may compromise protection against reinfection. Declining mucosal immunity, not antibody-dependent enhancement, may explain this reduced efficacy in offspring with high maternal antibodies (matAbs).

Area of Science:

  • Immunology
  • Virology
  • Pediatric Infectious Diseases

Background:

  • Respiratory syncytial virus (RSV) is a leading cause of severe respiratory illness and hospitalization in infants and young children.
  • Maternal vaccination is a strategy to confer passive immunity to newborns, offering protection against primary RSV infection.
  • The efficacy of maternal antibodies (matAbs) against secondary RSV infections in offspring remains poorly understood.

Purpose of the Study:

  • To evaluate the protective efficacy of maternal antibodies against RSV reinfection in offspring.
  • To investigate the mechanisms behind potentially exacerbated lung inflammation in offspring with high matAb levels following secondary RSV exposure.

Main Methods:

  • A mouse model was utilized involving maternal RSV vaccination followed by secondary RSV infection of offspring.
  • Offspring were categorized based on varying levels of maternal antibodies (matAbs) against RSV pre-F protein.
  • Lung pathology, gene expression (RSV-A N), inflammatory markers (IL-5, IL-13), MUC5AC, eosinophil markers (MBP), and antibody isotypes (sIgA, IgA, IgG) were assessed.

Main Results:

  • Offspring with high matAbs showed protection against primary RSV infection but experienced exacerbated lung pathology and weight loss upon reinfection.
  • Reinfection in high matAb offspring led to increased RSV-A N gene expression, eosinophilia, and elevated IL-5, IL-13, MUC5AC, and MBP.
  • A significant decline in secretory IgA (sIgA), mucosal IgA, and mucosal IgG was observed in high matAb offspring post-primary challenge, correlating with compromised secondary protection.

Conclusions:

  • Elevated maternal antibodies against RSV can compromise protection against secondary infection in offspring, contrary to initial protection.
  • The mechanism appears linked to a decline in mucosal immunity (sIgA, IgA, IgG) rather than antibody-dependent enhancement (ADE).
  • Findings highlight the need to consider mucosal immune responses and potential risks when developing maternal RSV vaccination strategies.

Keywords:
maternal immunizationmucosal immunityrespiratory syncytial virussecondary RSV exposuretype 2 inflammation

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