Pertussis vaccine antigens (aP antigens) (aP antigens)

Pertussis vaccine antigens are the primary active components of modern acellular pertussis (aP) vaccines, designed to provide protective immunity against Bordetella pertussis, the causative agent of whooping cough [10, 15]. These antigens typically consist of a combination of purified bacterial proteins, most commonly pertussis toxin (PT), filamentous hemagglutinin (FHA), pertactin (PRN), and fimbriae types 2 and 3 (FIM2/3) [2, 16]. PT is a major virulence factor that disrupts host cell signaling, while FHA, PRN, and FIM are critical adhesins that facilitate bacterial attachment to the ciliated respiratory epithelium [5, 18]. By presenting these specific proteins to the immune system, the vaccine elicits a targeted response involving the production of neutralizing antibodies and the activation of Th1, Th2, and Th17 cellular pathways [3, 10]. This immune response prevents the severe clinical manifestations of pertussis and aids in the clearance of the bacteria from the respiratory tract [1, 14]. Despite their high safety profile compared to older whole-cell vaccines, acellular antigens are associated with more rapid waning of immunity and have led to the selection of antigen-deficient escape strains in some populations [4, 12]. These antigens are almost exclusively administered as part of multivalent combination vaccines, such as DTaP for children and Tdap for adolescents and adults [8, 20].

Other names

Bordetella pertussis antigensAcellular pertussis antigensPertussis toxinFilamentous hemagglutininPertactinFimbriaeWhooping cough vaccine components

The mechanism of action involves the induction of an active immune response, where the body develops specific antibodies and memory T-cells against the included antigens [2]. Antibodies against pertussis toxin (PT) neutralize its systemic effects, while antibodies against adhesins like filamentous hemagglutinin (FHA), pertactin (PRN), and fimbriae (FIM) inhibit the attachment of Bordetella pertussis to the respiratory epithelium and promote bacterial clearance through opsonophagocytosis and complement-mediated lysis [1, 10].