胃幽門螺旋菌(Helicobacter pylori)是一種具鞭毛、微量需氧的革蘭氏陰性菌。在現今世界人口中約有一半的人遭受胃幽門螺旋菌的感染，並導致胃炎、胃潰瘍、十二指腸潰瘍、胃腺癌和胃癌等疾病。此菌寄生於胃上皮細胞，感染此菌所引起的胃部慢性發炎亦造成吞噬細胞於胃黏膜處的積聚。已知當胃幽門螺旋菌接觸到胃上皮細胞時，會將細胞膜上的膽固醇抽出並藉由capJ基因轉譯的膽固醇糖化轉移酵素(cholesterol--glucosyltransferase)形成醣化膽固醇(cholesteryl glucosides)以逃避寄主細胞的免疫反應。我們先前的研究中證明在被胃幽門螺旋菌感染的胃上皮細胞中，醣化膽固醇會影響寄主細胞膜的架構和第四型分泌系統(type IV secretion system)管柱的形成。在本研究中，我們用老鼠的巨噬細胞J774A.1探討胃幽門螺旋菌之醣化膽固醇對寄主細胞吞噬能力的影響。首先我們發現capJ基因剔除菌株(ΔcapJ H. pylori)在巨噬細胞內的存活率明顯的較野生型菌株(wild-type H. pylori)低。藉由活細胞影像共軛焦顯微鏡的拍攝和分析，顯示出與capJ基因剔除菌株相比，野生型菌株能延遲被巨噬細胞吞噬的時間；而剔除後又補回capJ基因的菌株(ΔcapJ-in H. pylori)則顯示出與野生型菌株相近似的平均被吞噬時間。同時，我們使用一種可偵測細胞內酸化胞器的LysoTracker Red染劑來追蹤進入溶小體(lysosome)的細菌，發現在相同的感染時間裡野生型菌株被送入溶小體的數量明顯的少於capJ基因剔除菌株。由以上的結果可推知胃幽門螺旋菌的CapJ蛋白具有延緩細菌被吞噬和延遲噬小體(phagosome)與溶小體融合的功能，因而使得細菌在吞噬細胞中的存活率增加。此外，藉由共軛焦顯微鏡的拍攝偵測初級內體(early endosome)和次級內體(late endosome)的標記物，我們發現在相同的感染時間裡野生型菌株被送入初級內體的數量高於capJ基因剔除菌株；但被送入次級內體的數量卻低於capJ基因剔除菌株。這個結果指出野生型菌株具有停滯吞噬小體運送(phagosome trafficking)並進而延緩噬小體與溶小體融合(phagolysosome)的功能。最後，經由預先對吞噬細胞處理不同的抑制物而後計數細胞內活菌數的實驗顯示野生型菌株而非capJ基因剔除菌株是透過脂質筏和PI3K相關的機制被送入吞噬細胞。本篇研究對於如何使巨噬細胞有效的吞噬胃幽門螺旋菌提供了一個新的視野，未來預期可將此新發現應用於治療胃幽門螺旋菌的感染。

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