ArticlePLoS pathogens2026
Cadherin-11 serves as a novel receptor for Fusobacterium nucleatum adhesin FadA to exacerbate pulmonary inflammation.
Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Fusobacterium nucleatum, a periodontal pathogen, has been increasingly implicated in pulmonary diseases including chronic obstructive pulmonary disease (COPD). This study demonstrates that F. nucleatum adheres to and invades pulmonary epithelial cells in a dose-dependent manner, primarily mediated by its adhesin FadA. We identify cadherin-11 (CDH11), which is upregulated in COPD lungs and in pulmonary epithelial cells treated with F. nucleatum or FadAc protein, as the key host receptor for FadA. This FadA-CDH11 interaction not only mediates bacterial adhesion and invasion, but also activates the MAPK13/JUN pathway, leading to significant upregulation of pro-inflammatory cytokines including CSF3, TNF-α, CCL20, and TGF-β. Genetic knockdown of CDH11 abolishes MAPK13/JUN activation and cytokine induction but does not affect FadA-mediated p53 suppression, indicating a separate pathway for this oncogenic event. Our findings establish the FadA-CDH11-MAPK13/JUN axis as a central mechanism driving F. nucleatum-exacerbated pulmonary inflammation and tissue damage, highlighting its potential as a therapeutic target for mitigating COPD progression.
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