A widely used steroid may be able to tame the harmful inflammation of a chronic lung infection without weakening the immune system’s ability to fight the organism.

Researchers at Trinity College Dublin and St. James’s Hospital studied dexamethasone in nontuberculous mycobacterial (NTM) infection — specifically Mycobacterium avium. Using infected human macrophages, they found dexamethasone reduced inflammatory signalling — lowering TNF, IL-6 and IL-1β — while preserving antimicrobial function, and did not increase bacterial burden over 120 hours. Published August 11, 2026 in The Journal of Infectious Diseases.

What NTM lung disease is

Nontuberculous mycobacteria are relatives of the organism causing tuberculosis, found widely in soil and water — including in domestic plumbing and shower heads. Most people encounter them without consequence.

In susceptible individuals — frequently those with existing lung damage from bronchiectasis, COPD or cystic fibrosis, and characteristically older, slender women without obvious predisposition — the organism establishes chronic infection.

Treatment is notoriously difficult: multiple antibiotics for a year or more beyond culture conversion, with substantial side effects and frequent failure or relapse. NTM infections are also rising in incidence across developed countries, for reasons not fully understood.

Why the damage is partly self-inflicted

Much of the lung damage comes from the body’s own inflammatory response rather than directly from the bacteria — a pattern shared with tuberculosis.

Mycobacteria survive inside macrophages, the very cells meant to destroy them, and the resulting standoff produces sustained inflammation. Over years, that inflammation destroys lung architecture, producing the bronchiectasis and cavitation that cause symptoms and progressive loss of function.

So a patient can be receiving effective antibiotics and continue to lose lung tissue to their own immune response.

The dilemma clinicians face

Steroids are powerful anti-inflammatories, and doctors hesitate to use them in infection for fear of blunting immune defences.

That caution is well founded generally. Corticosteroids increase susceptibility to infection, and steroid use is itself a recognised risk factor for developing NTM disease — so prescribing them to someone who already has it appears actively contraindicated.

Yet the inflammation is doing the damage, which leaves clinicians managing a condition where the obvious intervention is the one they are most reluctant to use.

What the study suggests can be separated

Dexamethasone throttled the cells’ inflammatory metabolism — glycolysis — while keeping their bacteria-killing machinery intact.

The metabolic detail is the mechanistic core. Activated macrophages switch to glycolysis, which supports the rapid production of inflammatory signals. Suppressing that switch reduces cytokine output.

Killing intracellular bacteria depends on different machinery — acidifying the compartment containing them, generating reactive species, and fusing it with degradative organelles. Those functions apparently do not require the same metabolic state.

“It may be possible to fine-tune this response by reducing damaging inflammation while still preserving the immune defenses that help control infection,” said researcher Donal Cox.

Why the bacterial burden result matters most

The finding that dexamethasone did not increase bacterial burden over 120 hours is the one that would change practice if it held.

It directly tests the fear driving clinical caution. If steroids suppressed macrophage killing, bacterial numbers would rise — and they did not, over five days in this system.

Five days is also the relevant limitation. Chronic infection unfolds over years, and an effect absent at 120 hours could emerge over months. Mycobacteria replicate slowly, so short experiments may simply not run long enough to detect a difference.

The precedent from tuberculosis

There is relevant clinical experience supporting the general idea. Corticosteroids are used alongside antibiotics in certain forms of tuberculosis — notably TB meningitis and pericarditis — where inflammation in a confined space causes damage that outweighs the risk of immune suppression.

That establishes the principle that steroids can be beneficial in mycobacterial infection under the right circumstances, which makes the NTM proposition less speculative than it first appears.

The limits

This is early, cell-based research. Isolated macrophages in culture lack everything else present in an infected lung — other immune cell types, tissue structure, the antibiotics patients are simultaneously taking, and the systemic effects steroids produce elsewhere in the body.

Systemic steroid effects are the practical obstacle. Even if the lung effect were exactly as described, long-term corticosteroid use causes bone loss, diabetes and infection risk elsewhere — so a benefit confined to inflammatory lung damage would need to outweigh harms distributed everywhere else.

Why NTM cases are rising

The increasing incidence of these infections is worth explaining, because it shapes how much a new management approach would matter.

Better detection accounts for part of it. CT scanning is more widely used, culture methods have improved, and clinicians are more aware of NTM as a diagnosis — so cases that would previously have been labelled as unexplained bronchiectasis or treatment-resistant chest infection are now identified.

Real increases appear to be occurring too. Populations are ageing, and NTM disease concentrates in older adults. More people are living with the chronic lung conditions that predispose to it, and more are immunosuppressed by medication for other diseases.

Environmental exposure may also have changed. These organisms thrive in warm water systems, and they resist the chlorine levels used in municipal supplies — so modern plumbing, showerheads and water heaters set to lower temperatures create favourable conditions. That combination of better recognition and genuinely more disease means the treatment problem is growing rather than merely becoming more visible.

Clinical studies would be needed before changing how these infections are managed. Early research; not medical advice.