White Jonathan Richard, Winter Jody Anne, Robinson Karen
NIHR Biomedical Research Unit in Gastrointestinal and Liver Diseases at Nottingham University Hospitals NHS Trust and The University of Nottingham, Nottingham, UK.
Interdisciplinary Biomedical Research Centre, School of Science and Technology, Nottingham Trent University, Nottingham, UK.
J Inflamm Res. 2015 Aug 13;8:137-47. doi: 10.2147/JIR.S64888. eCollection 2015.
The bacterial pathogen Helicobacter pylori commonly colonizes the human gastric mucosa during early childhood and persists throughout life. The organism has evolved multiple mechanisms for evading clearance by the immune system and, despite inducing inflammation in the stomach, the majority of infections are asymptomatic. H. pylori is the leading cause of peptic ulcer disease and gastric cancer. However, disease outcomes are related to the pattern and severity of chronic inflammation in the gastric mucosa, which in turn is influenced by both bacterial and host factors. Despite over 2 decades of intensive research, there remains an incomplete understanding of the circumstances leading to disease development, due to the fascinating complexity of the host-pathogen interactions. There is accumulating data concerning the virulence factors associated with increased risk of disease, and the majority of these have pro-inflammatory activities. Despite this, only a small proportion of those infected with virulent strains develop disease. Several H. pylori virulence factors have multiple effects on different cell types, including the induction of pro- and anti-inflammatory, immune stimulatory, and immune modulatory responses. The expression of multiple virulence factors is also often linked, making it difficult to assess the meaning of their effects in isolation. Overall, H. pylori is thought to usually modulate inflammation and limit acute damage to the mucosa, enabling the bacteria to persist. If this delicate balance is disturbed, disease may then develop.
细菌病原体幽门螺杆菌通常在儿童早期定植于人类胃黏膜，并终生持续存在。该生物体已进化出多种机制来逃避免疫系统的清除，尽管会在胃中引发炎症，但大多数感染是无症状的。幽门螺杆菌是消化性溃疡疾病和胃癌的主要病因。然而，疾病的发生与胃黏膜慢性炎症的模式和严重程度有关，而这又反过来受到细菌和宿主因素的影响。尽管经过了二十多年的深入研究，但由于宿主与病原体相互作用的惊人复杂性，对于导致疾病发展的情况仍未完全了解。关于与疾病风险增加相关的毒力因子的数据不断积累，其中大多数具有促炎活性。尽管如此，感染有毒力菌株的人中只有一小部分会发病。几种幽门螺杆菌毒力因子对不同细胞类型有多种影响，包括诱导促炎和抗炎、免疫刺激和免疫调节反应。多种毒力因子的表达也常常相互关联，使得难以孤立地评估它们作用的意义。总体而言，幽门螺杆菌通常被认为会调节炎症并限制对黏膜的急性损伤，从而使细菌得以持续存在。如果这种微妙的平衡被打破，疾病可能就会发生。
