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Fimbriae 2 and 3 are filamentous surface appendages produced by the bacterium Bordetella pertussis, the primary causative agent of whooping cough. These structures function as adhesins, facilitating the attachment of the pathogen to the ciliated respiratory epithelium of the host, which is a crucial step in colonization and infection (Mooi, 1988; Scheller & Cotter, 2015). Fimbriae 2 and 3 are major agglutinogens and are included as key antigenic components in several acellular pertussis (aP) vaccines to stimulate protective immunity (Edwards & Berbers, 2014). The expression of these proteins is controlled by the BvgAS regulatory system, and the bacteria can undergo phase variation or antigenic shift, potentially leading to the emergence of strains that lack specific fimbriae to evade vaccine-induced pressure (Zomer et al., 2014). Vaccination targeting these fimbriae aims to generate neutralizing antibodies that block bacterial adherence and promote clearance by the immune system.
Induction of antigen-specific antibodies (IgG) that inhibit bacterial adherence to respiratory epithelial cells and facilitate opsonophagocytosis.
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