University of Western Australia, Royal Perth Hospital, Perth, Western Australia, Australia.
Curr Opin Pulm Med. 2020 May;26(3):260-266. doi: 10.1097/MCP.0000000000000665.
Pulmonary nontuberculous mycobacterial disease (NTM) remains a significant clinical challenge with suboptimal therapy. This review focuses on recent understandings around the pathogenesis of NTM disease and nonantibiotic therapeutic approaches that are being pursued.
The absence of animal models that truly replicate human disease remains a major problem for NTM research with most findings coming from tuberculosis or tuberculosis-like studies. Recent research reiterates the known key roles of interferon gamma (IFNγ), tumor necrosis factor, interleukin-12 and granulocyte-macrophage colony stimulation factor (GM-CSF) in immunity to NTM. Autoantibodies to some of these factors may be important. Recent nonantibiotic research has focused on either boosting the immune response to NTM (e.g. with IFNγ or GM-CSF) or using other compounds to kill these pathogens (e.g. inhaled NO, gallium, etc.).
Our poor understanding of the immune deficit leading to NTM disease continues to hinder the development of highly effective therapies. New approaches are promising but need significant validation before being considered viable therapeutic options.
肺部非结核分枝杆菌病（NTM）的治疗仍然不理想，仍是一个重大的临床挑战。本综述重点介绍了 NTM 疾病发病机制和正在探索的非抗生素治疗方法的最新认识。
缺乏真正模拟人类疾病的动物模型仍然是 NTM 研究的一个主要问题，大多数发现来自于结核病或类似结核病的研究。最近的研究再次强调了干扰素 γ（IFNγ）、肿瘤坏死因子、白细胞介素 12 和粒细胞-巨噬细胞集落刺激因子（GM-CSF）在抗 NTM 免疫中的已知关键作用。针对这些因素中的一些自身抗体可能很重要。最近的非抗生素研究集中在增强对 NTM 的免疫反应（例如使用 IFNγ 或 GM-CSF）或使用其他化合物来杀死这些病原体（例如吸入一氧化氮、镓等）。
我们对导致 NTM 疾病的免疫缺陷的理解仍然很差，这继续阻碍了高效治疗方法的发展。新方法很有前途，但在被认为是可行的治疗选择之前，需要进行大量验证。
