# Fimbriae potentiate Aggregatibacter actinomycetemcomitans for periodontal disease

## TL;DR

This paper explains how fimbriae in Aggregatibacter actinomycetemcomitans contribute to periodontal disease and related conditions by enhancing virulence and immune evasion.

## Contribution

The paper reveals fimbriae's role in balancing surface structure and secretion-based virulence in A. actinomycetemcomitans.

## Key findings

- Fimbriae promote adhesion, biofilm formation, and immune evasion in A. actinomycetemcomitans.
- Fimbriated strains show reduced release of OMVs and ECPs compared to non-fimbriated strains.
- Fimbriae enhance the delivery of toxins like leukotoxin A, increasing pathogenicity.

## Abstract

•Aggregatibacter actinomycetemcomitans is a causative agent of periodontitis.•Fimbriae are key modulators of A. actinomycetemcomitans virulence.•Fimbriae drive aggregation, colonization, immune evasion and pathogenicity.•Fimbriae limit bacterial vesicle and extracellular cytoplasmic protein release.•Fimbriae are key therapeutic targets to control periodontal disease.

Aggregatibacter actinomycetemcomitans is a causative agent of periodontitis.

Fimbriae are key modulators of A. actinomycetemcomitans virulence.

Fimbriae drive aggregation, colonization, immune evasion and pathogenicity.

Fimbriae limit bacterial vesicle and extracellular cytoplasmic protein release.

Fimbriae are key therapeutic targets to control periodontal disease.

Aggregatibacter actinomycetemcomitans is a major contributor to aggressive periodontitis and has been increasingly implicated in systemic conditions, such as rheumatoid arthritis and Alzheimer’s disease. Among its diverse virulence mechanisms, fimbriae have emerged as central factors driving colonization, immune evasion, and pathogenicity. This review highlights recent findings showing that fimbriae not only facilitate adhesion and biofilm formation, but also contribute to maintaining bacterial cell envelope integrity. The transition from rough (fimbriated) to smooth (non-fimbriated) colony phenotypes upon in vitro culturing is associated with significant changes in virulence, including increased release of outer membrane vesicles (OMVs) and extracellular cytoplasmic proteins (ECPs). These changes suggest a trade-off between surface structure expression and secretion-based virulence. Importantly, fimbriae-rich strains are clinically relevant and more virulent in host models. The combined evidence implies that fimbriae and key virulence factors, such as leukotoxin A, act cooperatively in pathogenesis, as fimbriae-mediated adhesion and persistence will enhance local toxin delivery, killing of immune cells and immune evasion. Together, these insights point to fimbriae as key targets for novel therapeutic and vaccination strategies aimed at controlling periodontal and related systemic diseases.

Image, graphical abstract