# Inside Enemy Lines: Adhesion, Invasion, and Intracellular Persistence of Acinetobacter baumannii in the Respiratory Epithelium

**Authors:** Dolores Limongi, Daniela Scribano, Anna Teresa Palamara, Cecilia Ambrosi

PMC · DOI: 10.3390/pathogens15010102 · Pathogens · 2026-01-19

## TL;DR

This paper reviews how Acinetobacter baumannii infects and persists in respiratory cells, focusing on its adhesion, invasion, and immune evasion strategies.

## Contribution

The paper provides a comprehensive review of the diverse and redundant virulence mechanisms used by A. baumannii to establish intracellular infection.

## Key findings

- A. baumannii uses multiple strategies to adhere to and invade respiratory epithelial cells.
- The bacterium manipulates intracellular trafficking and evades immune defenses to persist within host cells.
- Clinical isolates show strain-specific differences in virulence and intracellular behavior.

## Abstract

Acinetobacter baumannii is a critical pathogen and a leading cause of hospital-acquired pneumonia, especially in immunocompromised patients. Although most research has focused on antimicrobial resistance, growing evidence shows that A. baumannii can efficiently adhere to, invade, and persist within human airway epithelial cells. Thus, the aim of this review is to summarize current knowledge on the mechanisms used by A. baumannii to establish infection, highlighting the bacterial traits responsible for attachment to airway epithelia, entry into host cells, manipulation of intracellular trafficking pathways to avoid degradation, metabolic adaptation to the host environment, and interference with immune defenses. The findings reported herein come from host–pathogen studies performed using epithelial cell lines, Galleria mellonella, and murine models, and from human primary airway cells. Despite the prominent role of the outer membrane protein OmpA, it is clear that A. baumannii pathogenicity relies on multiple, often redundant, virulence strategies to secure its intracellular niche and resist host pressures. Remarkably, strain heterogeneity in virulence traits between lab-domesticated and clinical isolates supports differential intracellular behavior and pathogenic potential. A deeper understanding of A. baumannii infection mechanisms is essential to design anti-virulence strategies that disarm this life-threatening bacterium, reduce selective pressure, limit resistance, and guide next-generation therapeutic interventions.

## Linked entities

- **Proteins:** ompa (olfactory marker protein a)
- **Diseases:** pneumonia (MONDO:0005249)
- **Species:** Acinetobacter baumannii (taxon 470), Galleria mellonella (taxon 7137), Mus musculus (taxon 10090)

## Full-text entities

- **Diseases:** infection (MESH:D007239), pneumonia (MESH:D011014)
- **Species:** Galleria mellonella (greater wax moth, species) [taxon 7137], Acinetobacter baumannii (species) [taxon 470], Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12845397/full.md

## References

163 references — full list in the complete paper: https://tomesphere.com/paper/PMC12845397/full.md

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Source: https://tomesphere.com/paper/PMC12845397