ArticleFrontiers in immunology2024
Neutrophil-derived Activin-A moderates their pro-NETotic activity and attenuates collateral tissue damage caused by Influenza A virus infection.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Proceedings of the 2Mediterranean journal of rheumatology · 2026Article
- Hippo pathway and NLRP3-driven NETosis in macrophages: Mechanisms of viral pneumoniaaggravation.Cell death discovery · 2025Article
- Transcriptomic analysis reveals shared deregulated neutrophil responses in COVID-19 and idiopathic pulmonary fibrosis.Respiratory research · 2025Article
- Neutrophil-fibroblast crosstalk drives immunofibrosis in Crohn's disease through IFNα pathway.Frontiers in immunology · 2024Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Background: Pre-neutrophils, while developing in the bone marrow, transcribe the Methods: To address this issue, we developed a neutrophil-specific Activin-A-deficient animal model ( Results: We found that neutrophil-specific Activin-A deficiency led to exacerbated pulmonary inflammation and widespread hemorrhagic histopathology in the lungs of IAV-infected animals that was associated with an exuberant production of neutrophil extracellular traps (NETs). Moreover, deletion of the Activin-A receptor ALK4/ACVR1B in neutrophils exacerbated IAV-induced pathology as well, suggesting that neutrophils themselves are potential targets of Activin-A-mediated signaling. The pro-NETotic tendency of Activin-A-deficient neutrophils was further verified in the context of thioglycollate-induced peritonitis, a model characterized by robust peritoneal neutrophilia. Of importance, transcriptome analysis of Activin-A-deficient neutrophils revealed alterations consistent with a predisposition for NET release. Conclusion: Collectively, our data demonstrate that Activin-A, secreted by neutrophils upon their activation in the periphery, acts as a feedback mechanism to moderate their pro-NETotic tendency and limit the collateral tissue damage caused by neutrophil excess activation during the inflammatory response.
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Registered trials
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