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Table · dataset · 2026

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<div> <p>Background</p><p>Gut epithelium serves as a critical barrier against <i>Trichinella spiralis</i> larval invasion, parasite-derived galectins are involved in host–parasite interactions, including invasion and immune modulation.

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This study investigated the role of <i>T. spiralis</i> galectin (Tsgal) in gut epithelial barrier disruption and larval invasion.</p> <p>Methodology/principal findings</p><p>Recombinant Tsgal (rTsgal) was expressed <i>in vitro</i> and its interaction with intestinal epithelial cells (IEC) was ascertained using immunofluorescence test (IFT) and confocal microscopy.

The rTsgal-specific binding IEC proteins were identified by GST pull-down, mass spectrometry (MS) and Co-immunoprecipitation (Co-IP) assay. Intestinal epithelial integrity damage induced by rTsgal was evaluated by IFT, qPCR and Western blotting analysis. The <i>in vitro</i> larva invasive assay was also conducted.

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The results showed that rTsgal bound and interacted specifically with MUC13 receptor in Caco-2 cells. rTsgal activated MUC13-ROCK2/MAPK pathway, reduced the expression of gut epithelial tight junctions (TJs; ZO-1, E-cad, Occludin and Claudin-1), increased gut epithelial permeability, disrupted gut epithelial integrity and barrier functions, thereby facilitated larva invasion of Caco-2 monolayers. Moreover, MUC13 receptor inhibitor (Cuc D), MUC13 knockdown of Caco-2 cells, ROCK2 inhibitor (KD025) and p38-MAPK inhibitor (SB203580) suppressed this pathway activation, restored gut epithelial integrity, and impeded larval invasion.</p> <p>Conclusions</p><p>Tsgal disrupted gut epithelial integrity and mediated larval invasion through binding to MUC13 receptor and activating ROCK2/MAPK pathway.

Tsgal might be a potential target molecule for development of novel drugs and vaccines to block <i>T. spiralis</i> infection.</p></div>

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