作者: Katharina Ronacher , Reinout van Crevel , Julia A. Critchley , Andrew A. Bremer , Larry S. Schlesinger
DOI: 10.1016/J.CHEST.2017.02.032
关键词:
摘要: There is growing interest in the re-emerging interaction between type 2 diabetes (DM) and TB, but underlying biologic mechanisms are poorly understood despite their possible implications clinical management. Experts epidemiologic, public health, basic science, studies recently convened identified research priorities for elucidating co-occurrence of TB DM. We gaps current knowledge altered immunity patients with DM during TB, where most suggest an underperforming innate immunity, but exaggerated adaptive to Mycobacterium tuberculosis. Various molecular pathways may underlie these observations host. These include signaling induced by excess advanced glycation end products receptor, higher levels reactive oxidative species stress, epigenetic changes due chronic hyperglycemia, nuclear receptors, and/or differences cell metabolism (immunometabolism). Studies humans at different stages (no DM, pre-DM, DM) or (latent active TB) should be complemented findings animal models, which provide unique opportunity study early events host-pathogen interaction. Such could also help identify biomarkers that will complement order tailor prevention TB-DM, avoid adverse treatment outcomes more likely patients. inform new approaches to host-directed therapies.