Menzies Health Institute Queensland, Griffith University, Southport, Australia.
Clem Jones Centre for Neurobiology and Stem Cell Research, Griffith University, Nathan, Australia.
PLoS Negl Trop Dis. 2020 Jan 24;14(1):e0008017. doi: 10.1371/journal.pntd.0008017. eCollection 2020 Jan.
The infectious disease melioidosis is caused by the bacterium Burkholderia pseudomallei. Melioidosis is characterised by high mortality and morbidity and can involve the central nervous system (CNS). We have previously discovered that B. pseudomallei can infect the CNS via the olfactory and trigeminal nerves in mice. We have shown that the nerve path is dependent on mouse strain, with outbred mice showing resistance to olfactory nerve infection. Damage to the nasal epithelium by environmental factors is common, and we hypothesised that injury to the olfactory epithelium may increase the vulnerability of the olfactory nerve to microbial insult. We therefore investigated this, using outbred mice that were intranasally inoculated with B. pseudomallei, with or without methimazole-induced injury to the olfactory neuroepithelium. Methimazole-mediated injury resulted in increased B. pseudomallei invasion of the olfactory epithelium, and only in pre-injured animals were bacteria found in the olfactory nerve and bulb. In vitro assays demonstrated that B. pseudomallei readily infected glial cells isolated from the olfactory and trigeminal nerves (olfactory ensheathing cells and trigeminal Schwann cells, respectively). Bacteria were degraded by some cells but persisted in other cells, which led to the formation of multinucleated giant cells (MNGCs), with olfactory ensheathing cells less likely to form MNGCs than Schwann cells. Double Cap mutant bacteria, lacking the protein BimA, did not form MNGCs. These data suggest that injuries to the olfactory epithelium expose the primary olfactory nervous system to bacterial invasion, which can then result in CNS infection with potential pathogenic consequences for the glial cells.
传染病类鼻疽由伯克霍尔德菌假单胞菌引起。类鼻疽的特点是高死亡率和发病率,并可涉及中枢神经系统(CNS)。我们之前发现,B. pseudomallei 可以通过嗅觉和三叉神经感染小鼠的中枢神经系统。我们已经表明,神经途径依赖于小鼠品系,杂种小鼠对嗅神经感染具有抗性。环境因素对鼻上皮的损伤很常见,我们假设嗅上皮的损伤可能会增加嗅神经对微生物侵袭的易感性。因此,我们使用经鼻腔接种 B. pseudomallei 的杂种小鼠进行了这项研究,其中一些动物的嗅神经上皮受到了甲巯咪唑诱导的损伤,而另一些则没有。甲巯咪唑介导的损伤导致 B. pseudomallei 更容易入侵嗅上皮,只有在预先受伤的动物中才会在嗅神经和球部发现细菌。体外试验表明,B. pseudomallei 容易感染从嗅觉和三叉神经分离的神经胶质细胞(分别为嗅鞘细胞和三叉神经施万细胞)。一些细胞可降解细菌,但在其他细胞中细菌仍能存活,这导致多核巨细胞(MNGC)的形成,嗅鞘细胞比施万细胞更不容易形成 MNGC。缺乏蛋白 BimA 的双帽突变细菌不会形成 MNGC。这些数据表明,嗅上皮的损伤使初级嗅觉神经系统容易受到细菌入侵,然后可能导致 CNS 感染,对神经胶质细胞产生潜在的致病性后果。