Tuberculosis (TB) bacteria can hide inside immune cells called macrophages, making treatment long and tough. Indian scientists found that the bacteria survive better when macrophages produce energy via oxidative phosphorylation (OXPHOS). But when macrophages switch to glycolysis, the bacteria become more vulnerable to antibiotics. The research team led by Dr. Amit Singh from IISc Bengaluru discovered that a protein called NRF2 helps bacteria survive by keeping macrophages in OXPHOS mode. Blocking NRF2 shifts metabolism to glycolysis and raises oxidative stress, weakening the bacteria. They tested meclizine, a widely used drug for nausea, which pushes macrophages to glycolysis. When combined with the frontline TB drug isoniazid, meclizine cut the bacterial load in mice by 20 times and aided lung recovery. This approach targets the host's metabolism, not the bacteria directly, which may reduce antibiotic resistance. Experts believe meclizine could improve TB treatment success and shorten treatment times if confirmed in human trials. Dr. Singh noted, "A drug combination including meclizine can activate the immune system, promote healing of the TB cavity, and restore lung function." The next step is to safely integrate meclizine with current TB drugs to prevent relapse and side effects. This discovery opens doors for host-directed therapies in fighting tough TB infections.