Ramarao N, Gray-Owen S D, Meyer T F
Max Planck Institute for Biology, Department of Infection Biology, Spemannstr. 34, 72076 Tübingen, Germany.
Mol Microbiol. 2000 Oct;38(1):103-13. doi: 10.1046/j.1365-2958.2000.02114.x.
Helicobacter pylori can colonize the gastric epithelium of humans, leading to the induction of an intense inflammatory response with the infiltration of mainly polymorphonuclear leucocytes (PMNs) and monocytes. These professional phagocytes appear to be a primary cause of the damage to surface epithelial layers, and probably contribute to the pathogenesis associated with persistent H. pylori infections. We have shown previously that H. pylori adheres to professional phagocytes, but is not engulfed efficiently, suggesting an antiphagocytic escape mechanism that is dependent on the pathogen's type IV secretion system. Here, we show that H. pylori induces the generation and extracellular release of oxygen metabolites as a consequence of its attachment to phagocytic cells, but is capable of surviving this response. The catalase activity of H. pylori is apparently essential for survival at the phagocytes' cell surface. Opsonization of H. pylori leads to an increased burst, and the inhibition of bacterial protein synthesis to a decreased one. Ca2+ concentration, cytoskeleton rearrangement and protein kinase C (PKC) are involved in the H. pylori-induced oxidative burst in both monocytes and PMNs. This survival phenomenon has important implications for both the persistence of this important pathogen and the host tissue damage that accompanies persistent H. pylori infection.
幽门螺杆菌可定植于人类胃上皮，引发强烈的炎症反应，主要有嗜中性粒细胞（PMNs）和单核细胞浸润。这些专业吞噬细胞似乎是表面上皮层损伤的主要原因，可能与幽门螺杆菌持续感染相关的发病机制有关。我们之前已表明，幽门螺杆菌可黏附于专业吞噬细胞，但不能被有效吞噬，这表明存在一种依赖病原体IV型分泌系统的抗吞噬逃逸机制。在此，我们表明幽门螺杆菌因其黏附于吞噬细胞而诱导氧代谢产物的生成和细胞外释放，但其能够在这种反应中存活。幽门螺杆菌的过氧化氢酶活性显然对于其在吞噬细胞表面的存活至关重要。幽门螺杆菌的调理作用导致爆发增加，而细菌蛋白质合成的抑制则导致爆发减少。Ca2+浓度、细胞骨架重排和蛋白激酶C（PKC）参与了幽门螺杆菌诱导的单核细胞和PMNs中的氧化爆发。这种存活现象对于这种重要病原体的持续存在以及幽门螺杆菌持续感染所伴随的宿主组织损伤均具有重要意义。
