fadA

FadA, short for Fusobacterium adhesion A, is a virulence-associated adhesin produced by Fusobacterium nucleatum, a Gram-negative bacterium commonly found in the human oral microbiome. As a surface-exposed protein, FadA functions as an adhesin and contributes to the bacterium’s ability to attach to host cells and establish infection.

In host cells, FadA mediates adhesion to epithelial surfaces and promotes invasion. The protein interacts with E-cadherin, a key component of adherens junctions, leading to disruption of cell–cell contacts and activation of signaling pathways. This engagement can trigger beta-catenin–dependent transcription and related inflammatory responses, with downstream effects on gene expression and cellular behavior. Experimental evidence indicates that FadA can modulate pathways such as Wnt/beta-catenin and NF-κB, contributing to an inflammatory environment and increased cellular permeability.

Biologically, FadA plays a role in oral biofilm formation and interbacterial interactions, aiding colonization and community development within dental plaque. Beyond the oral cavity, FadA-expressing F. nucleatum has been investigated for associations with colorectal cancer and other diseases, where laboratory studies suggest the adhesin may enhance tumor cell proliferation, inflammation, and tissue invasion. However, the extent of causality in humans remains an area of active research, and findings are interpreted within a broader context of microbial and host factors.

Research on FadA continues to explore its structure, regulation, and potential as a therapeutic target. Understanding how FadA contributes to adhesion and signaling helps illuminate mechanisms of Fusobacterium nucleatum–related pathology and points to strategies to mitigate bacterial colonization and associated inflammation.