Department of Biology, Shahed University, Tehran, Iran.
Department of Pathology, School of Medicine, Shahed University, Tehran, Iran.
APMIS. 2024 Nov;132(11):843-858. doi: 10.1111/apm.13465. Epub 2024 Sep 2.
BamA, an Omp85 superfamily member, is universally conserved and essential for cell viability. Using anti-Oma87 antibodies, we focus on understanding the effect of Oma87 of Acinetobacter baumannii on pathogenicity. Oma87 was expressed, purified, and used to induce anti-Oma87 antibodies in BALB/c mice. Acute toxicity of the protein was evaluated in mice. HeLa cells were infected with both live and killed A. baumannii 19606 and a clinical isolate. The effects of anti-Oma87 sera on A. baumannii adherence, internalization, and proliferation in HeLa cells were studied. The roles of microfilaments and microtubules in A. baumannii invasion were demonstrated by Actin disruption. Reduced bacterial population and biofilm formation were noted. The ability of A. baumannii to provoke autophagy through Oma87 induction leads to incomplete autophagy and potentially facilitates bacterial replication. Actin-mediated uptake, attachment, and invasion demonstrated A. baumannii survival and multiplication within vacuoles in the host cell. The findings underscore the potential of Oma87 as a therapeutic intervention target in infections caused by A. baumannii. This comprehensive analysis contributes valuable information for understanding the virulence mechanisms of A. baumannii, potentially guiding future strategies to combat infections caused by this pathogen.
BamA,一种 Omp85 超家族成员,普遍保守且对细胞活力至关重要。我们使用抗 Oma87 抗体,专注于了解鲍曼不动杆菌 Oma87 对致病性的影响。Oma87 被表达、纯化,并用于诱导 BALB/c 小鼠产生抗 Oma87 抗体。在小鼠中评估了该蛋白的急性毒性。HeLa 细胞被活的和已杀死的 A.baumannii 19606 和临床分离株感染。研究了抗 Oma87 血清对 HeLa 细胞中 A.baumannii 黏附、内化和增殖的影响。通过破坏微丝证明了微管在 A.baumannii 入侵中的作用。注意到细菌数量减少和生物膜形成减少。通过 Oma87 诱导,A.baumannii 引发自噬的能力导致不完全自噬,并可能促进细菌复制。肌动蛋白介导的摄取、附着和入侵表明 A.baumannii 在宿主细胞的空泡中存活和繁殖。这些发现强调了 Oma87 作为治疗干预鲍曼不动杆菌感染的靶标的潜力。这项全面分析为了解鲍曼不动杆菌的毒力机制提供了有价值的信息,可能为对抗这种病原体引起的感染提供未来的策略。