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Enterotoxigenic Escherichia coli F4 (ETEC F4), also known as K88, is a major virulence factor and a primary therapeutic target in the prevention of neonatal and post-weaning diarrhea in piglets [2, 8]. The F4 fimbriae are long, filamentous surface appendages that mediate the adherence of ETEC to specific glycoprotein or glycolipid receptors, such as Aminopeptidase N (APN) and MUC13, on the brush border of porcine intestinal epithelial cells [3, 10]. This adhesion is the critical first step in colonization, allowing the bacteria to proliferate and secrete enterotoxins that cause severe fluid loss and electrolyte imbalance [4, 7]. The F4 fimbria is composed of several subunits, with the major subunit FaeG acting as the primary adhesin responsible for receptor recognition [1, 5]. Therapeutic strategies targeting F4 include oral vaccines like Coliprotec F4 that induce mucosal immunity, monoclonal antibodies that block adhesion, and receptor analogs that competitively inhibit bacterial binding [6, 11]. Understanding the structural variants of F4 (F4ab, F4ac, and F4ad) and their corresponding host receptors is essential for developing broad-spectrum interventions against ETEC-related diseases in the swine industry [5, 12].
Inhibition of bacterial adhesion to the intestinal mucosa by neutralizing fimbrial adhesins or inducing protective mucosal IgA and IgG antibodies.
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