Department of Immunology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran; Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Immunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran; Department of Hematology and Laboratory Sciences, School of Para-Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Life Sci. 2019 Aug 15;231:116688. doi: 10.1016/j.lfs.2019.116688. Epub 2019 Jul 23.
The extended infection with Helicobacter pylori (H. pylori), one of the most frequent infectious agents in humans, may cause gastritis, peptic ulcers, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer. During H. pylori infection, different kinds of inflammatory cells such as dendritic cells, macrophages, neutrophils, mast cells, eosinophils, T cells and B cells are accumulated into the stomach. The interactions between chemokines and their respective receptors recruit particular types of the leukocytes that ultimately determine the nature of immune response and therefore, have a main influence on the consequence of infection. The suitable production of chemokines especially in the early stages of H. pylori infection shapes appropriate immune responses that contribute to the H. pylori elimination. The unbalanced expression of the chemokines can contribute in the induction of inappropriate responses that result in the tissue damage or malignancy. Thus, chemokines and their receptors may be promising potential targets for designing the therapeutic strategies against various types H. pylori-related gastrointestinal disorders. In this review, a comprehensive explanation regarding the roles played by chemokines in H. pylori-mediated peptic ulcer, gastritis and gastric malignancies was provided while presenting the potential utilization of these chemoattractants as therapeutic elements.
幽门螺杆菌（H. pylori）是人类最常见的感染病原体之一，长期感染可导致胃炎、消化性溃疡、胃黏膜相关淋巴组织（MALT）淋巴瘤和胃癌。在 H. pylori 感染过程中，不同类型的炎症细胞如树突状细胞、巨噬细胞、中性粒细胞、肥大细胞、嗜酸性粒细胞、T 细胞和 B 细胞聚集在胃中。趋化因子与其各自受体的相互作用招募特定类型的白细胞，最终决定免疫反应的性质，因此对感染的后果有主要影响。趋化因子的适当产生，特别是在 H. pylori 感染的早期阶段，可形成适当的免疫反应，有助于 H. pylori 的清除。趋化因子表达失衡可能导致不适当的反应，导致组织损伤或恶性肿瘤。因此，趋化因子及其受体可能是设计针对各种类型 H. pylori 相关胃肠道疾病的治疗策略的有前途的潜在靶点。在这篇综述中，详细阐述了趋化因子在 H. pylori 介导的消化性溃疡、胃炎和胃癌中的作用，并提出了将这些趋化因子作为治疗因子的潜在应用。
