ArticleFrontiers in immunology2016
Neutrophil Extracellular Traps Enhance Early Inflammatory Response in Sendai Virus-Induced Asthma Phenotype.
Article in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.
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Who cites it
27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.
- Characteristics and Role of Neutrophil Extracellular Traps in Asthma.Inflammation · 2022Pooled it
- In vitro induction of NETosis: Comprehensive live imaging comparison and systematic review.PloS one · 2017Pooled it
- Dipeptidyl peptidase-1 inhibition in patients hospitalised with COVID-19: a multicentre, double-blind, randomised, parallel-group, placebo-controlled trial.The Lancet. Respiratory medicine · 2022Trial
- Research progress on neutrophil extracellular traps in sepsis‑induced coagulopathy (Review).Molecular medicine reports · 2026Review
- Neutrophil extracellular traps in asthma and chronic obstructive pulmonary disease: pathogenic roles, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Cathepsin C-driven enhancement of neutrophil extracellular trap formation contributes to acute lung injury.iScience · 2025Article
- A citrullinated histone H3 monoclonal antibody for immune modulation in sepsis.Nature communications · 2025Article
- Exploring neutrophil extracellular traps: mechanisms of immune regulation and future therapeutic potential.Experimental hematology & oncology · 2025Review
- Neutrophil Extracellular Traps in Sepsis and Sepsis-Related Organ Dysfunction.ImmunoTargets and therapy · 2025Review
- Xiao Qing Long Tang ameliorates neutrophil extracellular trap-dendritic cells-T helper 17 cell axis in Neutrophilic Asthma.PloS one · 2025Article
- The role of innate immune system in respiratory viral infection related asthma.Frontiers in cellular and infection microbiology · 2025Review
- The role of extracellular traps released by neutrophils, eosinophils, and macrophages in asthma.Respiratory research · 2024Review
- Eosinophil extracellular traps in asthma: implications for pathogenesis and therapy.Respiratory research · 2023Review
- Neutrophil intrinsic and extrinsic regulation of NETosis in health and disease.Trends in microbiology · 2023Review
- Review
- Neutrophil extracellular traps in chronic lung disease: implications for pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Zingerone Inhibits the Neutrophil Extracellular Trap Formation and Protects against Sepsis via Nrf2-Mediated ROS Inhibition.Oxidative medicine and cellular longevity · 2022Article
- Neutrophils in respiratory viral infections.Mucosal immunology · 2021Review
- A sustained type I IFN-neutrophil-IL-18 axis drives pathology during mucosal viral infection.eLife · 2021Article
- Potentiation of NETs release is novel characteristic of TREM-1 activation and the pharmacological inhibition of TREM-1 could prevent from the deleterious consequences of NETs release in sepsis.Cellular & molecular immunology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Paramyxoviral infection in childhood has been linked to a significant increased rate of asthma development. In mice, paramyxoviral infection with the mouse parainfluenza virus type I, Sendai virus (Sev), causes a limited bronchiolitis followed by persistent asthma traits. We have previously shown that the absence of cysteine protease dipeptidyl peptidase I (DPPI) dampened the acute lung inflammatory response and the subsequent asthma phenotype induced by Sev. Adoptive transfer of wild-type neutrophils into DPPI-deficient mice restored leukocyte influx, the acute cytokine response, and the subsequent mucous cell metaplasia that accompanied Sev-induced asthma phenotype. However, the exact mechanism by which DPPI-sufficient neutrophils promote asthma development following Sev infection is still unknown. We hypothesize that neutrophils recruited to the alveolar space following Sev infection elaborate neutrophil extracellular traps (NETs) that propagate the inflammatory cascade, culminating in the eventual asthma phenotype. Indeed, we found that Sev infection was associated with NET formation in the lung and release of cell-free DNA complexed to myeloperoxidase in the alveolar space and plasma that peaked on day 2 post infection. Absence of DPPI significantly attenuated Sev-induced NET formation in vivo and in vitro. Furthermore, concomitant administration of DNase 1, which dismantled NETs, or inhibition of peptidylarginine deiminase 4 (PAD4), an essential mediator of NET formation, suppressed the early inflammatory responses to Sev infection. Lastly, NETs primed bone marrow-derived cells to release cytokines that can amplify the inflammatory cascade.
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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 OpenQuestion graph.