The following is a summary of “Paradoxical eosinophilic and cytokine responses to oral corticosteroid treatment in patients with asthma exacerbations,” published in the May 2024 issue of Allergy & Immunology by Maneechotesuwan, et al.

Thymic stromal lymphopoietin (TSLP) orchestrates eosinophilic inflammation, which may intensify during asthma exacerbations. Conversely, microRNA-1 (miR-1) inhibits TSLP-mediated eosinophil trafficking in lung endothelium. The relationship between the balance of TSLP and miR-1 levels and the response to oral corticosteroids (OCSs) during asthma exacerbation treatment needed to be better understood. For a study, researchers sought to explore the role of the TSLP/miR-1 axis in the inflammatory response to oral corticosteroid (OCS) treatment during asthma exacerbations.

They prospectively studied 28 consecutive patients with acute asthma exacerbations treated with prednisolone (30 mg/day) for one week in a real-life setting at the emergency department. Steroid responders were identified by a significant reduction in blood eosinophil counts, while paradoxical responders (PRs) either had no significant reduction or an increase in absolute blood eosinophil counts post-OCS treatment. Differential white blood cell counts, cytokine levels, and miR-1 expression were compared within and between groups before and after OCS treatment. Baseline cytokine concentrations in both groups were compared with those of patients with stable asthma.

OCS treatment significantly reduced TSLP levels in steroid responders (P = .006) but not in PRs (P = .742). miR-1 expression remained unchanged in steroid responders, while it significantly decreased in PRs despite being higher at baseline compared to patients with stable asthma, which may explain the slower resolution of exacerbations in PRs.

In asthmatic patients with acute exacerbations who did not show a decrease in eosinophil counts after a course of OCS, there was a paradoxical decrease in plasma miR-1 levels and an increase in TSLP levels compared to steroid responders. The imbalance may result in slower clinical recovery.

Reference: jaci-global.org/article/S2772-8293(24)00034-1/fulltext