ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
Group 2 innate lymphoid cells derived IL-9 reduces macrophage apoptosis and attenuates acute lung injury in sepsis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- The gut-lung axis in ARDS: beyond microbial translocation.Respiratory research · 2026Review
- Review
- Cytokine-mediated, organ-specific immune modulation and dysregulation of innate lymphocytes in sepsis.Seminars in immunopathology · 2026Review
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Letter to the Editor regarding "Ferroptosis is involved in the IL-9-induced intestinal barrier injury in sepsis: an experimental animal and translational study".International journal of surgery (London, England) · 2026Article
- Protective Effect of Low 2-O, 3-O Desulfated Heparin (ODSH) Against LPS-Induced Acute Lung Injury in Mice.Biomolecules · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
backgroundGroup 2 innate lymphoid cells (ILC2) are the main group of tissue-resident ILCs in the lungs, which protect airway barrier integrity following infection. Macrophages are integral to the regulation of immune homeostasis in sepsis. However, the relationship between ILC2 and macrophages in the context of sepsis induced acute lung injury remains uncertain.
methodsThe sepsis was conducted by cecal ligation and puncture (CLP) model in Wild Type (WT) mice and ILC2 depleted mice. Septic mice were injected intratracheally IL-9, and the frequency and markers expression of ILC2 and macrophage were measured by Flow cytometry and CyTOF. The lung injury was conducted with pathological analysis. In vitro studies, MH-S cells were exposed to LPS with/without interleukin-9 (IL-9), and mTOR level and MH-S cells death were measured with western bloting or Flow cytometry.
resultsSepsis induced the accumulation of ILCs and pulmonary macrophages in lungs. Furtherly, we revealed that ILC2 and CD45
conclusionsIL-9 secreted by ILC2 has a protective role in sepsis induced lung injury by reducing macrophage apoptosis and M1 polarization via mTOR.
Indexed as
Identifiers
39945866What Socratic holds
Registered trials
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 Socratic graph.