Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Int J Tuberc Lung Dis. 2019 Jun 1;23(6):669-677. doi: 10.5588/ijtld.18.0805.
People living with diabetes (DM) are at increased risk to become infected with , to progress from latent tuberculous infection to active tuberculosis (TB) disease, and to suffer adverse TB treatment outcomes. In some low- and middle-income countries, DM prevalence among newly diagnosed TB patients exceeds 40%. Despite the global significance of DM as an acquired TB risk factor, the biochemical and cellular mechanisms of susceptibility are incompletely understood. This review summarizes the landscape of basic research using animal models of the TB-DM interaction, and the extent to which findings in animal studies reflect or may explain the clinical features of TB-DM comorbidity in humans. We conclude that immunopathy results in damage to major organs as a complication of DM, likely operating through biochemical pathways such as those responsible for diabetic nephropathy, neuropathy, retinopathy, cardiovascular disease, and delayed wound healing. Insights gained from animal models can inform optimal management of TB-DM comorbidity and will be essential for pre-clinical development of therapeutic countermeasures.
患有糖尿病 (DM) 的人感染、从潜伏性结核感染发展为活动性结核病 (TB) 疾病以及遭受不利的 TB 治疗结局的风险增加。在一些低收入和中等收入国家，新诊断的 TB 患者中 DM 的患病率超过 40%。尽管 DM 作为获得性 TB 危险因素具有全球意义，但易感性的生化和细胞机制仍不完全清楚。这篇综述总结了使用 TB-DM 相互作用的动物模型进行的基础研究概况，以及动物研究中的发现在多大程度上反映或可以解释 TB-DM 合并症在人类中的临床特征。我们得出结论，免疫病理学导致 DM 并发症的主要器官损伤，可能通过负责糖尿病肾病、神经病、视网膜病变、心血管疾病和延迟伤口愈合的生化途径起作用。从动物模型中获得的见解可以为 TB-DM 合并症的最佳管理提供信息，并将是治疗对策的临床前开发的关键。
