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Fimbrial agglutinogen 3 (Fim3) is a major subunit of the type 3 fimbriae, which are filamentous surface appendages of the Gram-negative bacterium Bordetella pertussis [2, 14]. These structures function as critical adhesins, mediating the attachment of the pathogen to the ciliated respiratory epithelium of the host, which is a prerequisite for colonization and the development of whooping cough (pertussis) [7, 12, 13]. Fim3 is highly immunogenic and serves as a key antigen in several multi-component acellular pertussis vaccines (aP), such as Infanrix and Adacel, where it is often co-purified with Fim2 [3, 8]. Vaccines containing Fim3 induce the production of specific antibodies that block bacterial adhesion and promote clearance, thereby providing protection against infection [4, 9]. However, the prevalence of Fim3-expressing strains can fluctuate in response to vaccine-induced selective pressure, a phenomenon known as serotype switching, which poses a challenge for long-term vaccine efficacy [8, 10, 11]. This antigenic variation allows the bacteria to evade the host immune response, potentially contributing to the resurgence of pertussis in highly vaccinated populations [10, 15]. Consequently, Fim3 remains a focal point for the development of next-generation vaccines aimed at providing broader and more durable immunity [9, 11].
Vaccine-induced antibody-mediated inhibition of bacterial adhesion to host respiratory epithelium.
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