TY  - JOUR
N1  - Copyright of this article belongs to Elsevier BV
ID  - open3479
UR  - https://pmc.ncbi.nlm.nih.gov/articles/PMC13253091/
IS  - 6
A1  - Chaubey, Gaurav Kumar
A1  - Dilawari, Rahul
A1  - Modanwal, Radheshyam
A1  - Talukdar, Sharmila
A1  - Dhiman, Asmita
A1  - Patidar, Anil
A1  - Chaudhary, Surbhi
A1  - Sindhu, Anurag
A1  - Kumar, Ajay
A1  - Raje, Chaaya Iyengar
A1  - Raje, Manoj
Y1  - 2026/06/05/
N2  - Tuberculosis-diabetes comorbidity represents significant global health challenges, though the underlying mechanisms remain poorly understood. Mycobacterium tuberculosis (M.tb), the causative agent of tuberculosis, has a very high requirement of iron and its availability is a determining factor for successful establishment of infection. Host innate immune system and macrophages attempt to limit iron availability to restrict bacterial growth. We investigated the relationship between hyperglycemia and intracellular iron dynamics during infection using, THP-1-derived and primary macrophages from diabetic mice maintained under high-glucose conditions. Both showed increased intracellular iron along with higher expression of iron uptake receptors. Bacteria inside macrophages also contained more iron. Iron chelation significantly reduced M.tb burden in the lungs and spleen of infected diabetic mice. These findings suggest that hyperglycemia creates a ``glucose legacy'' that promotes iron accumulation, thereby increasing host susceptibility to M.tb infection, and reveals iron chelation as a promising adjunct therapeutic strategy.
PB  - Elsevier BV
JF  - iScience
VL  - 29
KW  - Immunology
TI  - Chronic hyperglycemia induces macrophage iron accumulation and promotes Mycobacterium tuberculosis virulence
ER  -