最近，由託馬斯傑弗遜大學，巴黎巴斯德研究所以及耶魯大學的研究人員組成的研究小組在PLoS ONE雜誌上發表了他們的研究成果，他們發現一些細胞內病原體能夠利用宿主細胞的生物學屬性來逃避細胞內溶酶體的攻擊和破壞。
導致女性不育的衣原體(Chlamydia)，引起軍團菌病的軍團菌(Legionella)等都是細胞內病原體，這些病原菌能夠躲避細胞內溶酶體的吞噬作用，但其具體的躲避機制研究人員一直都不甚了解。近日Fabienne Paumet等人發現，這種躲避機制可能與病原菌所表達的SNARE-like蛋白有關。
SNARE蛋白是真核細胞融合細胞內容物必需的蛋白質。這些蛋白一般以穩定的複合體形式出現在細胞內容物的表面，引發和細胞膜的融合。因此，衣原體和軍團菌必須和細胞內的運輸小泡以及細胞膜融合機制競爭，並且躲避溶酶體的破壞作用。
研究人員測試了病原菌所表達的SNARE-like蛋白，這些蛋白可以和真核細胞SNARE蛋白相互作用，並使細胞膜融合朝著利於病原菌生存的方向改變。衣原體和軍團菌表達的SNARE-like蛋白分別為IncA和IcmG/DotF，均能抑制真核細胞SNARE蛋白介導的細胞融合。
研究人員Dr. Paumet介紹說，根據觀察結果可以看出，細胞內病原體所表達的SNARE蛋白抑制劑能夠阻斷溶酶體和病原菌的融合。因此，這種SNARE-like蛋白或可成為治療諸如衣原體等這類病原微生物感染的新靶標。（生物谷Bioon.com）
生物谷推薦原始出處：
PLoS ONE 4(10): e7375. doi:10.1371/journal.pone.0007375
Intracellular Bacteria Encode Inhibitory SNARE-Like Proteins
Fabienne Paumet1*, Jordan Wesolowski1, Alejandro Garcia-Diaz2, Cedric Delevoye3, Nathalie Aulner4, Howard A. Shuman5, Agathe Subtil6, James E. Rothman2
1 Thomas Jefferson University, Department of Microbiology and Immunology, Philadelphia, Pennsylvania, United States of America, 2 Department of Cell Biology, Yale University, New Haven, Connecticut, United States of America, 3 Institut Curie, Structure et Compartiments Membranaires, CNRS-UMR144, Paris, France, 4 Institut Pasteur, Imagopole, Batiment Monod, Paris, France, 5 Department of Microbiology, Columbia University Medical Center, New York, New York, United States of America, 6 Institut Pasteur, Unité de Biologie des Interactions Cellulaires, CNRS-URA 2582, Paris, France
Pathogens use diverse molecular machines to penetrate host cells and manipulate intracellular vesicular trafficking. Viruses employ glycoproteins, functionally and structurally similar to the SNARE proteins, to induce eukaryotic membrane fusion. Intracellular pathogens, on the other hand, need to block fusion of their infectious phagosomes with various endocytic compartments to escape from the degradative pathway. The molecular details concerning the mechanisms underlying this process are lacking. Using both an in vitro liposome fusion assay and a cellular assay, we showed that SNARE-like bacterial proteins block membrane fusion in eukaryotic cells by directly inhibiting SNARE-mediated membrane fusion. More specifically, we showed that IncA and IcmG/DotF, two SNARE-like proteins respectively expressed by Chlamydia and Legionella, inhibit the endocytic SNARE machinery. Furthermore, we identified that the SNARE-like motif present in these bacterial proteins encodes the inhibitory function. This finding suggests that SNARE-like motifs are capable of specifically manipulating membrane fusion in a wide variety of biological environments. Ultimately, this motif may have been selected during evolution because it is an efficient structural motif for modifying eukaryotic membrane fusion and thus contribute to pathogen survival.