Fri Dec 19 02:30:00 UTC 2025: Okay, here’s a summary of the provided text and a rewritten version as a news article:

Summary:

A new study by Indian researchers published in Nature Communications suggests that improving TB treatment may not rely solely on new antibiotics, but on targeting and altering the metabolism of host macrophages. The study found that Mycobacterium tuberculosis (Mtb) survives within macrophages by manipulating their metabolism. When macrophages relied on oxidative phosphorylation (OXPHOS), Mtb could better neutralize oxidative stress and tolerate antibiotics. Conversely, when macrophages relied on glycolysis, Mtb was more susceptible to drugs. The researchers identified a regulatory molecule, NRF2, that plays a key role in this process. They then discovered that meclizine, an existing over-the-counter drug, could shift macrophage metabolism towards glycolysis, making Mtb more vulnerable to standard TB drugs. In mouse models, a combination of meclizine and isoniazid significantly reduced bacterial load and showed signs of lung tissue recovery. The findings suggest that host-directed therapies like meclizine could offer a promising approach to shorten treatment duration, combat drug resistance, and improve patient outcomes by promoting lung healing.

News Article:

Existing Motion Sickness Drug Shows Promise in Shortening TB Treatment, Indian Researchers Find

Pune, India – December 19, 2025 – A breakthrough study led by Indian researchers has identified a novel approach to combating tuberculosis (TB), potentially revolutionizing treatment protocols and offering hope for shorter, more effective therapies. The research, published in Nature Communications, suggests that targeting the metabolism of immune cells called macrophages, rather than solely focusing on new antibiotics, could be the key to overcoming TB’s resilience.

For months, Mycobacterium tuberculosis (Mtb), the bacteria responsible for TB, can persist within macrophages, the very cells designed to destroy them. Researchers have found that Mtb manipulates macrophage metabolism to create a protected niche, leading to lengthy treatment regimens and increased drug resistance.

The study revealed that Mtb’s drug tolerance is directly linked to the metabolic state of the macrophage. When macrophages relied on oxidative phosphorylation (OXPHOS), Mtb was better able to neutralize oxidative stress and evade antibiotics. However, when macrophages relied on glycolysis, the bacteria became more vulnerable. Researchers identified a key regulatory molecule, NRF2, that influences this metabolic shift.

Intriguingly, the team discovered that meclizine, a readily available over-the-counter drug commonly used for motion sickness, could effectively redirect macrophage metabolism towards glycolysis. This metabolic switch significantly increased Mtb’s susceptibility to existing frontline TB drugs.

In mouse models mimicking human TB, a combination of isoniazid and meclizine produced a staggering 20-fold decrease in bacterial load compared to isoniazid alone. Furthermore, the lungs of meclizine-treated animals showed signs of tissue recovery, addressing a critical unmet need as many TB survivors suffer from long-term lung damage.

“This observation opens up avenues to identify additional host-targeting compounds that have the potential for switching macrophage metabolism to a drug susceptible state, and can synergise with conventional anti-TB drugs that target the bacterium,” said Raghunand R. Tirumalai, a senior scientist at the CSIR-Centre for Cellular and Molecular Biology, who was not involved in the study.

The research team, led by Amit Singh of the Indian Institute of Science, Bengaluru, is optimistic about the potential of host-directed therapies like meclizine to improve treatment outcomes, combat drug resistance, and promote lung healing.

“In addition to improving treatment efficacy, a drug combination including meclizine can activate the immune system, promote healing of the TB cavity, and restore lung function,” Dr. Singh said.

The next step involves conducting clinical trials in humans to determine the optimal dosage and safety profile of meclizine in combination with existing TB treatments. If successful, this approach could significantly shorten treatment durations, improve patient adherence, reduce TB transmission, and curb the rise of drug-resistant strains. The fact that meclizine crosses the blood-brain barrier also raises the possibility that it could improve outcomes in TB patients with central nervous system infections.

The study underscores the importance of exploring innovative strategies that target the host-pathogen interaction to combat infectious diseases. These findings offer a ray of hope in the global fight against TB, a disease that continues to plague millions worldwide.

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