Over a quarter of the world’s population is infected with Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB). Approximately 3.4% of new and 18% of recurrent cases of TB are multidrug-resistant (MDR) or rifampicin-resistant. Recent evidence has shown that certain drug-resistant strains of Mtb modulate host metabolic reprogramming, and therefore immune responses, during infection. However, it remains unclear how widespread these mechanisms are among circulating MDR Mtb strains and what impact drug-resistance-conferring mutations have on immunometabolism during TB. While few studies have directly addressed metabolic reprogramming in the context of drug-resistant Mtb infection, previous literature examining how drug-resistance mutations alter Mtb physiology and differences in the immune response to drug-resistant Mtb provides significant insights into how drug-resistant strains of Mtb differentially impact immunometabolism.

超过四分之一的世界人口感染了结核分枝杆菌( Mtb )，它是结核病 (TB) 的病原体。大约 3.4% 的新结核病例和 18% 的复发结核病例是耐多药 (MDR) 或耐利福平。最近的证据表明，某些Mtb耐药菌株在感染期间调节宿主代谢重编程，从而调节免疫反应。然而，目前尚不清楚这些机制在循环 MDR Mtb菌株中的普遍程度以及赋予耐药性的突变对 TB 期间的免疫代谢有什么影响。虽然很少有研究直接解决耐药Mtb背景下的代谢重编程感染，先前的文献研究抗药性突变如何改变的Mtb生理和药物抗性的免疫应答的差异的Mtb提供显著洞察如何耐药菌株的Mtb差异影响immunometabolism。