Omp34-Mediated Invasion of Human Cervical Carcinoma Epithelial, HeLa Cells, and the Influence of Anti-Omp34 Antibodies.

is known for its ability to invade and persist within eukaryotic cells, impacting infection outcomes and disease progression. This study investigates the role of Omp34, a key outer membrane protein (Omp), in interaction with epithelial cells and the protective effects of anti-Omp34 antibodies (Abs). Omp34 is a key regulator of epithelial cell invasion, influencing bacterial adherence, internalization, and intracellular proliferation. The presence of anti-Omp34 Abs mitigates -induced cellular damage and enhances bacterial clearance. The process involved the expression and purification of Omp34, which in turn induced Abs in BALB/c mice against Omp34. The acute toxicity of Omp34 was studied through a histological analysis conducted on six distinct organs in mice. HeLa cells were infected by ATCC 19606 and a clinical strain. Various aspects of behavior with HeLa cells, including HeLa cell viability, adherence, serum resistance, cell internalization, and intracellular proliferation with and without anti-Omp34 sera. Cytoskeleton inhibitors were used to study the potential roles played in the process of invasion by microfilaments and microtubules. Omp34 effectively triggered Ab production in mice without resulting in any toxicity. The assay for serum resistance revealed potent bactericidal and antibiofilm effects on both strains. Bacterial internalization was constrained when actin polymerization was inhibited. Examination under the microscope revealed instances of adherence, alterations in the cell membrane, apoptosis, vacuolization, and cell damage. HeLa cells exposed to anti-Omp34 serum showed decreased cell damage. The results provide substantial evidence of the adherence capacity of to proliferate in the epithelial cells. In conclusion, Omp34 plays a substantial role in regulating interactions between epithelial cells and , the multifaceted nature of which intricately modifies the trajectory of infection within host cells by .