Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2025 Oct 1;31(5):575-581.
doi: 10.1097/MCC.0000000000001303. Epub 2025 Jul 7.

Acute respiratory distress syndrome: new pathophysiological insights

Affiliations
Review

Acute respiratory distress syndrome: new pathophysiological insights

Asyl Harbiye et al. Curr Opin Crit Care. .

Abstract

Purpose of review: Acute respiratory distress syndrome (ARDS) remains a major cause of critical illness with high morbidity and mortality. Despite advances in supportive care, targeted therapies have failed, in part due to an incomplete understanding of alveolar immune dysregulation. This review provides a timely synthesis of emerging mechanisms in alveolar immune dysregulation that underlie the development and persistence of ARDS.

Recent findings: Recent studies highlight the role of neutrophil heterogeneity, alveolar macrophage-derived extracellular vesicle signaling, and epithelial barrier dysfunction in driving hyperinflammation and susceptibility to secondary infections. Mechanical ventilation strategies, particularly those influencing driving pressure, further shape the alveolar immune environment. Cross-talk between immune cells and mechanical forces appears central to the pathogenesis of sustained lung injury.

Summary: Understanding the dynamic interplay between alveolar immune responses and secondary insults is critical for the development of precision medicine approaches in ARDS. Future research should prioritize the identification of compartment-specific biomarkers and therapeutic targets aimed at restoring immune balance and preventing nonresolving lung injury.

Keywords: acute respiratory distress syndrome; alveolar immunity; extracellular vesicles; secondary infections; ventilator-induced lung injury.

PubMed Disclaimer

References

    1. Bos LDJ, Ware LB. Acute respiratory distress syndrome: causes, pathophysiology, and phenotypes. Lancet 2022; 400:1145–1156.
    1. Bellani G, Laffey JG, Pham T, et al. Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA 2016; 315:788–800.
    1. Calfee CS, Delucchi K, Parsons PE, et al. Subphenotypes in acute respiratory distress syndrome: latent class analysis of data from two randomised controlled trials. Lancet Respir Med 2014; 2:611–620.
    1. Bos LD, Schouten LR, van Vught LA, et al. Identification and validation of distinct biological phenotypes in patients with acute respiratory distress syndrome by cluster analysis. Thorax 2017; 72:876–883.
    1. Calfee CS, Delucchi KL, Sinha P, et al. Acute respiratory distress syndrome subphenotypes and differential response to simvastatin: secondary analysis of a randomised controlled trial. Lancet Respir Med 2018; 6:691–698.

MeSH terms

LinkOut - more resources