Steroid Curbs Chronic Lung Inflammation Without Weakening Immune Defenses

A new study published in The Journal of Infectious Diseases reveals that dexamethasone, a common anti-inflammatory steroid, can reduce inflammatory signaling in human macrophages infected with Mycobacterium avium, without weakening the cells' ability to control bacterial growth. The research, led by Trinity College Dublin and St. James’s Hospital, suggests dexamethasone could serve as a host-directed strategy for managing nontuberculous mycobacterial disease, which often persists despite antibiotic treatment.

The team examined human monocyte-derived macrophages, immune cells that act as the body's first line of defense against infection, and found that while M. avium infection triggers a glycolytic response in macrophages, dexamethasone dampens this metabolic shift without altering oxygen consumption. Crucially, dexamethasone did not increase bacterial loads over a 120-hour period, indicating the steroid does not compromise antimicrobial defenses.

The researchers observed a significant reduction in the production of pro-inflammatory cytokines TNF, IL-6, IL-8, and IL-1β in macrophages treated with dexamethasone, though the anti-inflammatory effects remained broad, including an impact on IL-10 production at higher doses. The findings support further investigation into using dexamethasone as a means to limit inflammation while preserving host defense mechanisms in patients with nontuberculous mycobacterial disease.

However, the researchers emphasize the need for additional studies in more relevant models of NTM disease, including alveolar macrophages and clinical M. avium isolates, before dexamethasone can be considered as an adjunct therapy for chronic NTM lung disease.