Balest Alessandra, Peracino Barbara, Bozzaro Salvatore
Department of Clinical and Biological Sciences; University of Turin; Orbassano, Italy.
Commun Integr Biol. 2011 Mar;4(2):194-7. doi: 10.4161/cib.4.2.14381.
Recently we reported that Dictyostelium cells ingest Legionella pneumophila by macropinocytosis, whereas other bacteria, such as Escherichia coli, Mycobacterium avium, Neisseria meningitidis or Salmonella typhimurium, are taken up by phagocytosis.1 In contrast to phagocytosis, macropinocytosis is partially inhibited by PI3K or PTEN inactivation, whereas both processes are sensitive to PLC inhibition. Independently from reduced uptake, L. pneumophila proliferates more efficiently in PI3K-null than in wild-type cells. PI3K inactivation also neutralizes resistance to infection conferred by constitutively expressing the endo-lysosomal iron transporter Nramp1. We have shown this to be due to altered recruitment of the V-H(+) ATPase, but not Nramp1, in the Legionella-containing vacuole (LCV) early during infection.1 As further evidence for impaired LCV acidification we examine here the effects of disrupting the small G protein RacH on Legionella infection.
最近我们报道，盘基网柄菌细胞通过巨胞饮作用摄取嗜肺军团菌，而其他细菌，如大肠杆菌、鸟分枝杆菌、脑膜炎奈瑟菌或鼠伤寒沙门氏菌，则通过吞噬作用被摄取。1与吞噬作用不同，巨胞饮作用会被PI3K或PTEN失活部分抑制，而这两个过程都对PLC抑制敏感。与摄取减少无关，嗜肺军团菌在PI3K基因敲除细胞中比在野生型细胞中增殖更有效。PI3K失活还能消除组成型表达内溶酶体铁转运蛋白Nramp1所赋予的抗感染能力。我们已经证明，这是由于感染早期含军团菌液泡（LCV）中V-H(+)ATP酶（而非Nramp1）的募集改变所致。1作为LCV酸化受损的进一步证据，我们在此研究破坏小G蛋白RacH对军团菌感染的影响。
