乙醯基胺葡萄糖水解酶於胃幽門桿菌感染胃癌細胞扮演之角色

Abstract

全球約有50%人口身上帶有胃幽門螺旋桿菌感染。在相關醫學研究中，已確立胃幽門桿菌之感染為導致腸胃道疾病如胃炎、胃潰瘍及胃癌的主要原因之一，雖然已有許多研究揭露胃幽門桿菌的致病機制，但對於在感染中宿主細胞與胃幽門桿菌之間詳細的互動機制仍不甚清楚。先前本實驗室發現胃幽門桿菌之感染會促使宿主細胞分泌出第二型岩藻醣水解酶，且此酵素可加強胃幽門桿菌附著於宿主細胞的能力，在感染及致病過程中扮演重要角色。本研究中進一步發現，另一種糖解酵素-乙醯胺基葡萄糖水解酶亦存在於胃幽門桿菌感染宿主細胞的狀況下。與未感染的對照組比較，不論是以原生型或是由臨床病人身上分離的胃幽門桿菌感染宿主細胞，共同培養液中的乙醯胺基葡萄糖水解酶活性都會顯著提高。此外，乙醯胺基葡萄糖水解酶於實驗中具有抑制胃幽門桿菌生長之作用。雖目前尚未釐清何種因子會造成此酵素的釋放，以及此酵素透過何種機制影響胃幽門桿菌的存活，這些發現仍進一步地揭露了胃幽門桿菌與宿主細胞於感染過程中的交互作用。

Infection about one half of the global population, the bacterial pathogen H. pylori is the primary cause of gastritis, duodenal ulcer and gastric cancer. Despite the well-known infection mechanism, the interactions between H. pylori and the host during infection are not fully understood. We previously identified α-L-fucosidase to be secreted from host cells upon H. pylori infection. The enzyme is connected to the bacterial adhesion, growth and pathogenicity of the pathogen. Here we report the presence of another glycosidase, N-acetyl-β-D-hexosaminidase, under co-culture conditions, but with a different scenario. In comparison with a negative control (no infection, the level of β-hexosaminidase activity was greatly enhanced upon the infection of H. pylori strains, including wild type and other clinical isolates. In addition, the presence of β-hexosaminidase significantly reduced the viability of H. pylori in vitro. Although it still remain unclear about what factors contribute to the release of β-hexosaminidase, and how the enzyme affects the bacterial survival, this study provides another example of host-pathogen interaction.