New findings open doors for adjunctive steroid therapy in TB care
Tuberculosis (TB) remains a global health challenge, affecting more than 10 million people each year. A new study published in Scientific Reports suggests that carefully targeted use of steroids could serve as a universal complementary treatment to bolster the body’s defense against TB while reducing inflammatory damage. The research focuses on how steroids influence macrophages, the immune cells that play a crucial role in controlling TB infection.
How steroids affect macrophages and TB bacteria
Glucocorticoids like dexamethasone are already used in TB care, particularly in severe manifestations such as TB meningitis. However, their broader impact on immune cell function has not been fully understood. The new study reveals that dexamethasone can dampen glycolysis in macrophages—reducing the energy supply available to the cells. At the same time, it modulates cytokine production, decreasing both pro-inflammatory and anti-inflammatory signals measured in their experiments.
These dual actions may seem paradoxical at first: lowering inflammation could protect tissues from damage, but energy reduction and altered signaling might also constrain the immune system’s ability to fight the bacteria. The researchers found, intriguingly, that dexamethasone simultaneously tempering inflammation and preserving antimicrobial defense can occur, offering a potential optimal balance in TB treatment.
Evidence from macrophage experiments
Researchers analyzed macrophages derived from healthy volunteers’ blood and, in some cases, from lung fluid donated from patients undergoing routine bronchoscopies. By infecting these macrophages with Mycobacterium tuberculosis (Mtb) in the lab and applying dexamethasone, they tracked changes in the cells’ ability to control infection and survive the assault of the bacteria.
Results showed that Mtb-infected macrophages treated with dexamethasone exhibited increased survival, suggesting a complex interaction between the drug and cellular fate during infection. Crucially, the team also observed a reduction in bacterial burden within these infected macrophages. This improvement appears to be linked, at least in part, to autophagy and phagosomal acidification—processes by which cells degrade and clear intracellular pathogens.
Implications for TB treatment strategies
The findings lend support to using steroids as an adjunct alongside standard antimicrobial therapies, particularly in TB cases characterized by excessive or damaging inflammatory responses. By dampening harmful inflammation while preserving, or even enhancing, the macrophages’ capacity to kill bacteria, dexamethasone could help improve patient outcomes without compromising antimicrobial defense.
Expert commentary from Prof Joseph Keane of Trinity College Dublin highlights the practical significance: “In clinical practice, steroids are the most underused adjunctive therapy for TB. We often rely on steroids to manage inflammation in tuberculosis, particularly in severe forms like TB meningitis. What’s reassuring from this study is that dexamethasone not only tempers inflammation but also appears to support the macrophage’s ability to control infection.”
What comes next for TB care and research
While the lab-based results are compelling, translating them into standardized clinical protocols will require careful trials to determine optimal dosing, timing, and patient selection. The goal is to harness the protective benefits of steroids against excessive inflammatory damage while maintaining strong antimicrobial activity to reduce bacterial load.
As researchers refine these insights, clinicians may gain a valuable addition to TB care—one that complements antibiotics and improves health outcomes for millions affected by the disease worldwide.
