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Minor fimbrial protein Mfa1 is the major structural subunit of the minor (short) fimbriae of Porphyromonas gingivalis, a keystone pathogen in chronic periodontitis [1, 2]. These fimbriae are essential for the bacterium's ability to adhere to host tissues and co-aggregate with other oral bacteria, such as Streptococcus gordonii, to form pathogenic biofilms [7, 13]. Mfa1 also interacts with host immune receptors like TLR2 and DC-SIGN, contributing to the inflammatory response and the pathogen's persistence [6, 13]. Because of its critical role in colonization and virulence, Mfa1 is a primary target for the development of vaccines, monoclonal antibodies, and small-molecule inhibitors aimed at preventing or treating periodontal disease and its associated systemic complications [4, 14]. Experimental therapies, including monoclonal antibodies and peptide-based inhibitors, have shown efficacy in reducing bacterial load and alveolar bone loss in animal models [8, 14].
Inhibition of bacterial adhesion and biofilm formation by blocking Mfa1-mediated interactions with host cells and commensal bacteria [9, 14].
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