Targeting BamA, the essential component of the β-barrel assembly machinery, hinders its ability to adhere to and invade human alveolar basal epithelial cell line.

The lungs are commonly targeted by . The human alveolar basal epithelial cell line, A549, serves as a valuable in vitro model for probing pathogen-cell dynamics. This study examined two Acinetobacter strains, ATCC 19606 and the clinical isolate 58ST, investigating their adherence, internalization, and cytotoxicity within the A549 cell line to illuminate pathogenic mechanisms. Anti-BamA antibodies were expressed, purified, and detected via indirect ELISA. The toxicity of BamA was assessed across BALB/c mice. Both strains were used to infect A549 cells to scrutinize cell invasion diversity. Serum resistance, biofilm creation and inhibition, adhesion, internalization, and intracellular proliferation of live and inactivated were probed with and without anti-BamA sera. A549 cell viability was evaluated in the presence of live and anti-BamA sera-exposed bacteria. Cytoskeleton inhibitor tests were conducted on epithelial cells. strains displayed differing cell invasion aptitudes, with the clinical variant manifesting the highest invasion capability. During internalization, cells localized within vacuoles and migrated towards the nucleus using a zipper-like invasion mechanism. Bacterial division inside host cells culminated in cell demise. Pre-treatment with anti-BamA antibodies substantially impeded 's adherence and invasion in epithelial cells. Microscopic imaging validated the intracellular presence of in A549 cells, verifying their invasive potential and residency. These findings substantiate 's capacity to proliferate in epithelial cells, with BamA pivotal role against -epithelial cell interplay. This study augments our insight into pathogenesis, facilitating the development of efficacious strategies against infections.