科學(xué)家們鑒別出一種新蛋白質(zhì),，這種蛋白質(zhì)能探測和控制那些逃離宿主防御系統(tǒng)的細菌,。他們在日前在線出版的《自然—免疫學(xué)》期刊上報道,，這種蛋白質(zhì)與高度致病性細菌的去除有關(guān),。
盡管有害的細菌一般均會隱蔽在人體宿主細胞中的一個隔間中,，如導(dǎo)致傷寒和腸胃炎的沙門氏菌,，但這些細菌也會偶爾逃離這個隔間并侵入宿主細胞,。因尚未查明的原因,，這些逃離的細菌通常會披上宿主蛋白質(zhì)泛素。
Felix Randow和同事發(fā)現(xiàn),，宿主蛋白質(zhì)NDP52與這些披上泛素外衣的細菌捆綁在一起,，應(yīng)要求消滅入侵的細菌,。通過征集其他的宿主防御蛋白質(zhì)，NDP52好像促進了細菌的自我吞噬,。當然,，還需要做進一步的工作以精確確定，究竟有多少致病性細胞受NDP52控制,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Immunology 10, 1215 - 1221 (2009) 11 October 2009 | doi:10.1038/ni.1800
The TBK1 adaptor and autophagy receptor NDP52 restricts the proliferation of ubiquitin-coated bacteria
Teresa L M Thurston1,3, Grigory Ryzhakov1,2,3, Stuart Bloor1,3, Natalia von Muhlinen1 & Felix Randow1
Cell-autonomous innate immune responses against bacteria attempting to colonize the cytosol of mammalian cells are incompletely understood. Polyubiquitylated proteins can accumulate on the surface of such bacteria, and bacterial growth is restricted by Tank-binding kinase (TBK1). Here we show that NDP52, not previously known to contribute to innate immunity, recognizes ubiquitin-coated Salmonella enterica in human cells and, by binding the adaptor proteins Nap1 and Sintbad, recruits TBK1. Knockdown of NDP52 and TBK1 facilitated bacterial proliferation and increased the number of cells containing ubiquitin-coated salmonella. NDP52 also recruited LC3, an autophagosomal marker, and knockdown of NDP52 impaired autophagy of salmonella. We conclude that human cells utilize the ubiquitin system and NDP52 to activate autophagy against bacteria attempting to colonize their cytosol.
1 Medical Research Council Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Cambridge, UK.
2 Present address: Kennedy Institute of Rheumatology, Imperial College London, London, UK.
3 These authors contributed equally to this work.
