Gillette-Ferguson Illona, Hise Amy G, McGarry Helen F, Turner Joseph, Esposito Andrew, Sun Yan, Diaconu Eugenia, Taylor Mark J, Pearlman Eric
Department of Ophthalmology, Case Western Reserve University, Cleveland, Ohio 44106-4983, USA.
Infect Immun. 2004 Oct;72(10):5687-92. doi: 10.1128/IAI.72.10.5687-5692.2004.
Endosymbiotic Wolbachia bacteria are abundant in the filarial nematodes that cause onchocerciasis (river blindness), including the larvae (microfilariae) that migrate into the cornea. Using a mouse model of ocular onchocerciasis, we recently demonstrated that it is these endosymbiotic bacteria rather than the nematodes per se that induce neutrophil infiltration to the corneal stroma and loss of corneal clarity (Saint Andre et al., Science 295:1892-1895, 2002). To better understand the role of Wolbachia organisms in the pathogenesis of this disease, we examined the fate of these bacteria in the cornea by immunoelectron microscopy. Microfilariae harboring Wolbachia organisms were injected into mouse corneas, and bacteria were detected with antibody to Wolbachia surface protein. Within 18 h of injection, neutrophils completely surrounded the nematodes and were in close proximity to Wolbachia organisms. Wolbachia surface protein labeling was also prominent in neutrophil phagosomes, indicating neutrophil ingestion of Wolbachia organisms. Furthermore, the presence of numerous electron-dense granules around the phagosomes indicated that neutrophils were activated. To determine if Wolbachia organisms directly activate neutrophils, peritoneal neutrophils were incubated with either parasite extracts containing Wolbachia organisms, parasite extracts depleted of Wolbachia organisms (by antibiotic treatment of worms), or Wolbachia organisms isolated from filarial nematodes. After 18 h of incubation, we found that isolated Wolbachia organisms stimulated production of tumor necrosis factor alpha and CXC chemokines macrophage inflammatory protein 2 and KC by neutrophils in a dose-dependent manner. Similarly, these cytokines were induced by filarial extracts containing Wolbachia organisms but not by Wolbachia-depleted extracts. Taken together, these findings indicate that neutrophil activation is an important mechanism by which Wolbachia organisms contribute to the pathogenesis of ocular onchocerciasis.
内共生沃尔巴克氏体细菌在导致盘尾丝虫病(河盲症)的丝虫线虫中大量存在,包括迁移至角膜的幼虫(微丝蚴)。利用眼部盘尾丝虫病小鼠模型,我们最近证明,正是这些内共生细菌而非线虫本身,诱导中性粒细胞浸润至角膜基质并导致角膜透明度丧失(圣安德烈等人,《科学》295:1892 - 1895,2002年)。为了更好地理解沃尔巴克氏体微生物在该疾病发病机制中的作用,我们通过免疫电子显微镜检查了这些细菌在角膜中的命运。将携带沃尔巴克氏体微生物的微丝蚴注射到小鼠角膜中,并用抗沃尔巴克氏体表面蛋白的抗体检测细菌。注射后18小时内,中性粒细胞完全包围了线虫,并与沃尔巴克氏体微生物紧密相邻。沃尔巴克氏体表面蛋白标记在中性粒细胞吞噬体中也很突出,表明中性粒细胞摄取了沃尔巴克氏体微生物。此外,吞噬体周围存在大量电子致密颗粒,表明中性粒细胞被激活。为了确定沃尔巴克氏体微生物是否直接激活中性粒细胞,将腹膜中性粒细胞与含有沃尔巴克氏体微生物的寄生虫提取物、去除了沃尔巴克氏体微生物的寄生虫提取物(通过用抗生素处理蠕虫)或从丝虫线虫中分离出的沃尔巴克氏体微生物一起孵育。孵育18小时后,我们发现分离出的沃尔巴克氏体微生物以剂量依赖的方式刺激中性粒细胞产生肿瘤坏死因子α以及CXC趋化因子巨噬细胞炎性蛋白2和KC。同样,这些细胞因子由含有沃尔巴克氏体微生物的丝虫提取物诱导产生,但不由去除了沃尔巴克氏体的提取物诱导产生。综上所述,这些发现表明中性粒细胞激活是沃尔巴克氏体微生物促成眼部盘尾丝虫病发病机制的重要机制。