ArticleAmerican journal of respiratory and critical care medicine2026
Interleukin-6 is a mediator of therapeutic efficacy in acute lung injury.
Article in American journal of respiratory and critical care medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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10 authors.
Funding
Abstract
rationaleInflammation in acute respiratory distress syndrome (ARDS) and COVID-19 causes disruption of the alveolar-capillary barrier and tissue damage, which has been associated with increased mortality. Elevated pro-inflammatory plasma biomarker (specifically IL-6) levels reflect the degree of systemic inflammation and are linked to severity of lung injury. Understanding the causal pathway between inflammation, interventions, and patient outcomes could improve clinical care.
objectivesTo assess IL-6 as a mediator of effective interventions in ARDS and COVID-19.
methodsWe leveraged individual patient data from 5 large randomized controlled trials. Interventions were imatinib, anakinra, low tidal volume ventilation, high positive end-expiratory pressure (PEEP), and simvastatin. We evaluated IL-6 as a mediator for the effectiveness of interventions on 28-day survival with joint modeling. Additionally, we analyzed the role of other pro-inflammatory markers (IL-8, tumor necrosis factor receptor 1, and C-reactive protein). The association between IL-6 and mortality was meta-analyzed using a random effects model. MEASUREMENTS AND MAIN
resultsFor 2563 patients, IL-6 measures were available at baseline and at least 1 other timepoint. Interleukin-6 mediated the effects of imatinib, anakinra, and low tidal volume on mortality. Higher PEEP and simvastatin did not alter IL-6 trajectories. In all studies, there were associations between higher IL-6 concentrations and increased mortality over 28 days (pooled hazard ratio [HR] for a log10-unit increase = 4.83, 95% CI, 3.50-6.66).
conclusionsThe mortality benefit by anakinra and imatinib in COVID-19 and low tidal volume ventilation in acute lung injury may operate through resolution of inflammation defined by a reduction in plasma IL-6 levels.
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