ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Enhanced resolution of experimental ARDS through IL-4-mediated lung macrophage reprogramming.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 105 citations in OpenAlex.
- Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Emerging roles of basophils in the resolution of acute respiratory distress syndrome.The European respiratory journal · 2025Article
- Alveolar and Bone Marrow-derived Macrophages Differ in Metabolism and Glutamine Utilization.American journal of respiratory cell and molecular biology · 2025Article
- Metabolic Regulation in Acute Respiratory Distress Syndrome: Implications for Inflammation and Oxidative Stress.International journal of chronic obstructive pulmonary disease · 2025Review
- Bioactive Nanomaterials: Comprehensive Monitoring and Regulation of Acute Pancreatitis Induced Acute Lung Injury.International journal of nanomedicine · 2025Review
- The dichotomic role of cytokines in aging.Biogerontology · 2024Review
- Macrophages modulate skeletal muscle wasting and recovery in acute lung injury in mice.Physiological reports · 2024Article
- A GPCR-neuropeptide axis dampens hyperactive neutrophils by promoting an alternative-like polarization during bacterial infection.Immunity · 2024Article
- 11β hydroxysteroid dehydrogenase type 1 transgenic mesenchymal stem cells attenuate inflammation in models of sepsis.Frontiers in bioengineering and biotechnology · 2024Article
- IL-4/IL-4 Ab complex enhances the accumulation of both antigen-specific and bystander CD8 T cells in mouse lungs infected with influenza A virus.Laboratory animal research · 2023Article
- Advantages and disadvantages of treatment of experimental ARDS by M2-polarized RAW 264.7 macrophages.Heliyon · 2023Article
- Differences in Mortality Among Patients With Asthma and COPD Hospitalized With COVID-19.The journal of allergy and clinical immunology. In practice · 2023Article
- Pseudomonas-dominant microbiome elicits sustained IL-1β upregulation in alveolar macrophages from lung transplant recipients.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2023Article
- Mechanisms and Effects of Macrophage Polarization and Its Specifics in Pulmonary Environment.Physiological research · 2023Review
- DNA methyltransferase inhibition induces dynamic gene expression changes in lung CD4Scientific reports · 2023Article
- The Role of Macrophages and Alveolar Epithelial Cells in the Development of ARDS.Inflammation · 2023Review
- Impaired alveolar macrophage 11β-hydroxysteroid dehydrogenase type 1 reductase activity contributes to increased pulmonary inflammation and mortality in sepsis-related ARDS.Frontiers in immunology · 2023Article
- Integrative proteomic profiling of lung tissues and blood in acute respiratory distress syndrome.Frontiers in immunology · 2023Article
- Absence of CCR2 Promotes Proliferation of Alveolar Macrophages That Control Lung Inflammation in Acute Respiratory Distress Syndrome in Mice.International journal of molecular sciences · 2022Article
- Lack of STAT6 enhances murine acute lung injury through NLRP3/p38 MAPK signaling pathway in macrophages.BMC immunology · 2022Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
Despite intense investigation, acute respiratory distress syndrome (ARDS) remains an enormous clinical problem for which no specific therapies currently exist. In this study, we used intratracheal lipopolysaccharide or Pseudomonas bacteria administration to model experimental acute lung injury (ALI) and to further understand mediators of the resolution phase of ARDS. Recent work demonstrates macrophages transition from a predominant proinflammatory M1 phenotype during acute inflammation to an anti-inflammatory M2 phenotype with ALI resolution. We tested the hypothesis that IL-4, a potent inducer of M2-specific protein expression, would accelerate ALI resolution and lung repair through reprogramming of endogenous inflammatory macrophages. In fact, IL-4 treatment was found to offer dramatic benefits following delayed administration to mice subjected to experimental ALI, including increased survival, accelerated resolution of lung injury, and improved lung function. Expression of the M2 proteins Arg1, FIZZ1, and Ym1 was increased in lung tissues following IL-4 treatment, and among macrophages, FIZZ1 was most prominently upregulated in the interstitial subpopulation. A similar trend was observed for the expression of macrophage mannose receptor (MMR) and Dectin-1 on the surface of alveolar macrophages following IL-4 administration. Macrophage depletion or STAT6 deficiency abrogated the therapeutic effect of IL-4. Collectively, these data demonstrate that IL-4-mediated therapeutic macrophage reprogramming can accelerate resolution and lung repair despite delayed use following experimental ALI. IL-4 or other therapies that target late-phase, proresolution pathways may hold promise for the treatment of human ARDS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.