Hilda J Nancy, Narasimhan Meenakshi, Das Sulochana D
Department of Immunology, National Institute for Research in Tuberculosis, Chetput, Chennai 600031, India.
Institute for Thoracic Medicine, Chetput, Chennai 600031, India.
Hum Immunol. 2014 Aug;75(8):914-22. doi: 10.1016/j.humimm.2014.06.020. Epub 2014 Jun 30.
Neutrophils being innate cells initiate the immune defence against mycobacteria by sending signals to other immune cells. Chemokines being the vital link in signaling processes, it is of interest to study their secretion by neutrophils as a response to tuberculosis infection. The levels of various chemokines (MIP-1α, MCP-1, IL-8 and IP-10) and chemokine receptors (CXCR1, CXCR2 and CCR1) in neutrophils from healthy individuals and pulmonary tuberculosis patients were studied following infection with Mycobacterium tuberculosis strains (clinical--S7 and S10 and laboratory--H37Rv). The release of MIP-1α, IL-8 and MCP-1 is found to be greatly increased in patient neutrophils. Mycobacterial strains differentially influenced neutrophils affecting the release of chemokines to different extent. H37Rv significantly increased the release of MIP-1α and IL-8 in both normals and tuberculosis patients, while S10 up regulated only the release of MIP-1α in patients. Thus, during tuberculosis, neutrophils undergo functional alteration to combat infection. While H37Rv is greatly recognized by neutrophils and triggers the release of chemokines, clinical strains by some means try to suppress immune activation of neutrophils in their favor.
中性粒细胞作为先天免疫细胞，通过向其他免疫细胞发送信号来启动针对分枝杆菌的免疫防御。趋化因子是信号传导过程中的关键环节，因此研究中性粒细胞对结核感染的反应而分泌趋化因子具有重要意义。我们研究了健康个体和肺结核患者的中性粒细胞在感染结核分枝杆菌菌株（临床菌株——S7和S10以及实验室菌株——H37Rv）后，各种趋化因子（MIP-1α、MCP-1、IL-8和IP-10）和趋化因子受体（CXCR1、CXCR2和CCR1）的水平。结果发现，患者中性粒细胞中MIP-1α、IL-8和MCP-1的释放量大幅增加。分枝杆菌菌株对中性粒细胞有不同影响，在不同程度上影响趋化因子的释放。H37Rv显著增加了正常人和肺结核患者中MIP-1α和IL-8的释放，而S10仅上调了患者中MIP-1α的释放。因此，在结核病期间，中性粒细胞会发生功能改变以对抗感染。虽然H37Rv能被中性粒细胞高度识别并触发趋化因子的释放，但临床菌株会通过某种方式试图抑制中性粒细胞的免疫激活，使其有利于自身。
