Virulent strains of Helicobacter pylori demonstrate delayed phagocytosis and stimulate homotypic phagosome fusion in macrophages.
Virulent strains of Helicobacter pylori demonstrate delayed phagocytosis and stimulate homotypic phagosome fusion in macrophages.
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DOI：
10.1084/jem.191.1.115
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发表时间：
2000-01-03
期刊：
影响因子：
--
通讯作者：
Kang B
中科院分区：
文献类型：
--
作者：
Allen LA;Schlesinger LS;Kang B
幽门螺杆菌定植于世界上约50%人口的胃上皮，并在胃溃疡和十二指肠溃疡的发展中起致病作用。H.幽门螺杆菌被单核吞噬细胞吞噬，但内化的细菌没有被杀死，这种宿主防御缺陷的原因尚不清楚。我们现在使用免疫荧光和电子显微镜显示，H。幽门螺杆菌采用一种不寻常的机制来避免吞噬细胞的杀伤：延迟进入，随后是同型吞噬体融合。未经处理的I型H。pylori很容易与巨噬细胞结合，并在104分钟后被内化为富含肌动蛋白的吞噬体。pylori吞噬体在接下来的12小时内聚结。所得的“巨体”含有多种活的生物体，并且稳定24 h。吞噬体-吞噬体融合需要细菌蛋白质合成和完整的宿主微管，氯霉素和诺考达唑都增加了对细胞内H.幽门螺杆菌。H.幽门螺杆菌毒性较低，并且缺乏CAG致病岛。与I型菌株相反，II型H. pylori的细胞被巨噬细胞迅速摄取和杀死，并且不刺激巨体形成。总的来说，我们的数据表明，巨体的形成是一个重要的特点，H。pylori发病机制
Helicobacter pylori colonizes the gastric epithelium of ∼50% of the world's population and plays a causative role in the development of gastric and duodenal ulcers. H. pylori is phagocytosed by mononuclear phagocytes, but the internalized bacteria are not killed and the reasons for this host defense defect are unclear. We now show using immunofluorescence and electron microscopy that H. pylori employs an unusual mechanism to avoid phagocytic killing: delayed entry followed by homotypic phagosome fusion. Unopsonized type I H. pylori bound readily to macrophages and were internalized into actin-rich phagosomes after a lag of ∼4 min. Although early (10 min) phagosomes contained single bacilli, H. pylori phagosomes coalesced over the next ∼2 h. The resulting “megasomes” contained multiple viable organisms and were stable for 24 h. Phagosome–phagosome fusion required bacterial protein synthesis and intact host microtubules, and both chloramphenicol and nocodazole increased killing of intracellular H. pylori. Type II strains of H. pylori are less virulent and lack the cag pathogenicity island. In contrast to type I strains, type II H. pylori were rapidly ingested and killed by macrophages and did not stimulate megasome formation. Collectively, our data suggest that megasome formation is an important feature of H. pylori pathogenesis.
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DOI：
10.1083/jcb.124.5.677
发表时间：
1994-03
期刊：
The Journal of cell biology
影响因子：
--
作者：
Desjardins M;Huber LA;Parton RG;Griffiths G
通讯作者：
Griffiths G
影响因子：
1.9
作者：
FIOCCA, R;LUINETTI, O;SOLCIA, E
通讯作者：
SOLCIA, E
DOI：
10.1111/j.1574-695x.1994.tb00472.x
发表时间：
1994-06-01
影响因子：
--
作者：
CHMIELA, M;LELWALAGURUGE, J;WADSTROM, T
通讯作者：
WADSTROM, T
DOI：
10.1083/jcb.137.1.113
发表时间：
1997-04-07
期刊：
The Journal of cell biology
影响因子：
--
作者：
Blocker A;Severin FF;Burkhardt JK;Bingham JB;Yu H;Olivo JC;Schroer TA;Hyman AA;Griffiths G
通讯作者：
Griffiths G
影响因子：
1.9
作者：
Bukholm, G;Tannaes, T;Guldvog, I
通讯作者：
Guldvog, I