Rethinking Mycoplasma hyopneumoniae adhesion: a glycocalyx-mediated infectious niche model in porcine respiratory infection.

Abstract

Mycoplasma hyopneumoniae (Mhp) is the primary etiological agent of porcine enzootic pneumonia and establishes infection through close association with the respiratory ciliated epithelium. Classical models of Mhp colonization have focused mainly on specific interactions between adhesins, particularly P97, and ciliary receptors. Although this framework has provided important insights into ciliary attachment, increasing evidence indicates that Mhp adhesion involves multiple surface proteins and host ligands, including sulfated glycosaminoglycans (GAGs), fibronectin, plasminogen (Plg) and extracellular actin. In this review, we synthesize current evidence and propose a glycocalyx-mediated infectious niche framework for early Mhp colonization. Within this framework, sulfated glycans within the respiratory glycocalyx may contribute to bacterial positioning at the airway interface, while multiligand adhesin interactions may contribute to attachment and Plg-binding surface proteins may facilitate host-factor recruitment. Among these interactions, plasminogen recruitment provides a potential link between adhesion and local interface modification, including possible extracellular matrix remodeling and epithelial injury. Other processes, including potential GAG-mediated local retention, host glycan-dependent variation in attachment and glycocalyx remodeling, remain hypotheses requiring further validation. By distinguishing experimentally supported interactions from mechanistic inferences, this review presents Mhp colonization as a dynamic host-pathogen interface process rather than a simple adhesin-receptor event. This framework provides a basis for future investigation of early colonization mechanisms and anti-adhesion strategies in porcine enzootic pneumonia.