Department of Microbiology and Immunology, University of Texas Medical Branch Galveston, Texas, United States of America.
Department of Pathology, University of Texas Medical Branch Galveston, Texas, United States of America.
PLoS Negl Trop Dis. 2024 Oct 15;18(10):e0012585. doi: 10.1371/journal.pntd.0012585. eCollection 2024 Oct.
Burkholderia pseudomallei (Bpm) is the causative agent of the disease melioidosis. As a facultative intracellular pathogen, Bpm has a complex lifestyle that culminates in cell-to-cell fusion and multinucleated giant cells (MNGCs) formation. The virulence factor responsible for MNGC formation is the type 6 secretion system (T6SS), a contractile nanomachine. MNGC formation is a cell-to-cell spread strategy that allows the bacteria to avoid the extracellular immune system and our previous data highlighted cell death, apoptosis, and inflammation as pathways significantly impacted by T6SS activity. Thusly, we investigated how the T6SS influences these phenotypes within the macrophage and pulmonary models of infection. Here we report that the T6SS is responsible for exacerbating apoptotic cell death during infection in both macrophages and the lungs of infected mice. We also demonstrate that although the T6SS does not influence differential macrophage polarization, the M2 polarization observed is potentially beneficial for Bpm pathogenesis and replication. Finally, we show that the T6SS contributes to the severity of inflammatory nodule formation in the lungs, which might be potentially connected to the amount of apoptosis that is triggered by the bacteria.
类鼻疽伯克霍尔德菌(Bpm)是类鼻疽病的病原体。作为一种兼性细胞内病原体,Bpm 具有复杂的生活方式,最终导致细胞融合和多核巨细胞(MNGCs)的形成。导致 MNGC 形成的毒力因子是类型 6 分泌系统(T6SS),这是一种收缩纳米机器。MNGC 的形成是一种细胞间传播策略,使细菌能够逃避细胞外免疫系统,我们之前的数据强调了细胞死亡、细胞凋亡和炎症是 T6SS 活性显著影响的途径。因此,我们研究了 T6SS 如何在感染的巨噬细胞和肺部模型中影响这些表型。在这里,我们报告 T6SS 负责加剧感染期间巨噬细胞和感染小鼠肺部中细胞凋亡的发生。我们还证明,尽管 T6SS 不影响巨噬细胞的极化差异,但观察到的 M2 极化可能有利于 Bpm 的发病机制和复制。最后,我们表明 T6SS 导致肺部炎症性结节形成的严重程度增加,这可能与细菌触发的细胞凋亡量有关。