Max Planck Institute for Infection Biology, Department of Immunology, Berlin, Germany.
Curr Opin Immunol. 2013 Aug;25(4):441-9. doi: 10.1016/j.coi.2013.05.005. Epub 2013 May 28.
Inflammation is critical for tuberculosis (TB) pathogenesis. The nonresolving aspect of inflammation in TB is caused by sophisticated intracellular survival strategies of tubercle bacilli. TB is a continuum comprising a spectrum of lesions as a consequence of complex regulation of inflammation. Proinflammatory cytokines, including interferons, tumor necrosis factor and interleukin 1 along with microRNAs and eicosanoids form an interactive network during TB. Cross-regulation between proinflammatory mediators strongly impacts on infected cell death patterns. These processes, in concert with local concentrations of proteases, such as cathepsins, serpins and matrix-metalloproteinases, affect tissue integrity, shape the architecture of granulomas and modulate tissue repair. With inflammation networks being uncovered in TB, the relevance of several pathways for novel interventions becomes clearer.
炎症对于结核病（TB）的发病机制至关重要。导致 TB 炎症无法解决的原因是结核分枝杆菌复杂的细胞内生存策略。TB 是一个连续体，包含一系列病变，是炎症复杂调控的结果。促炎细胞因子，包括干扰素、肿瘤坏死因子和白细胞介素 1，以及 microRNAs 和类二十烷酸，在 TB 期间形成一个相互作用的网络。促炎介质之间的交叉调节强烈影响受感染细胞的死亡模式。这些过程与组织蛋白酶、丝氨酸蛋白酶抑制剂和基质金属蛋白酶等局部蛋白酶浓度一起，影响组织完整性、塑造肉芽肿结构并调节组织修复。随着在 TB 中发现炎症网络，几个通路对于新的干预措施的相关性变得更加清晰。
