Department of Infectious, Parasitic and Immune-Mediated Diseases, 00161 Rome, Italy.
J Microbiol. 2009 Dec;47(6):768-73. doi: 10.1007/s12275-009-0103-0. Epub 2010 Feb 4.
The pathogenesis of Legionella pneumophila mainly resides in its ability to inhibit the phagosome-lysosome fusion, which normally prevents the killing of the host cells. In order to characterize the molecular alterations that occurred in a spontaneous avirulent mutant of Legionella pneumophila serogroup 6, named Vir-, we investigated the ability of the mutant to adhere to and multiply in the WI26VA4 alveolar epithelial cell line and in human macrophages, when compared to its parental strain, Vir+. We also determined the colocalization of bacteria with LAMP-1 to gain an insight into the phagosome-lysosome fusion process. Additionally, we determined the flagellin expression and dotA nucleotide sequencing. We observed a lack of expression of flagellin and an in-frame mutation in the dotA. gene. The data obtained strongly suggest the loss of virulence of the mutant could probably be due to the absence of flagellin and the dysfunctional type IV secretion System, resulting from the DotA protein being severely compromised.
嗜肺军团菌的发病机制主要在于其抑制吞噬体-溶酶体融合的能力，这通常可防止宿主细胞被杀死。为了描述军团菌血清型 6 的一种自发无毒突变体 Vir-发生的分子变化，我们研究了该突变体与亲本菌株 Vir+相比，在 WI26VA4 肺泡上皮细胞系和人巨噬细胞中黏附和增殖的能力。我们还确定了细菌与 LAMP-1 的共定位，以深入了解吞噬体-溶酶体融合过程。此外，我们还确定了鞭毛蛋白的表达和 dotA 核苷酸序列。我们观察到鞭毛蛋白表达缺失和 dotA 基因中的框内突变。这些数据强烈表明，突变体毒力的丧失可能是由于鞭毛蛋白缺失和功能失调的 IV 型分泌系统所致，这是由于 DotA 蛋白严重受损所致。
