ArticleThorax2018
Neutrophils drive alveolar macrophage IL-1β release during respiratory viral infection.
Article in Thorax, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 77 citations in OpenAlex.
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- Targeting alveolar macrophages: a promising intervention for pulmonary infection and acute lung injury.Cellular & molecular biology letters · 2025Review
- Jinxin oral liquid reduced lung inflammation in influenza A virus infected mice through inhibiting NOD-like receptor protein 3 pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Absence of c-Maf and IL-10 enables type I IFN enhancement of innate responses to LPS in alveolar macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
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- TLR7 Promotes Acute Inflammatory-Driven Lung Dysfunction in Influenza-Infected Mice but Prevents Late Airway Hyperresponsiveness.International journal of molecular sciences · 2024Article
- Monocyte-Derived Macrophages Induce Alveolar Macrophages Death via TNF-α in Acute Lung Injury.Immunity, inflammation and disease · 2024Article
- The role of alveolar macrophages in viral respiratory infections and their therapeutic implications.Biochemistry and biophysics reports · 2024Review
- Exposure to bacterial PAMPs before RSV infection exacerbates innate inflammation and disease via IL-1α and TNF-α.Mucosal immunology · 2024Article
- Absence of c-Maf and IL-10 enables Type I IFN enhancement of innate responses to low-dose LPS in alveolar macrophages.bioRxiv : the preprint server for biology · 2024Article
- Targeting the TRAF3-ULK1-NLRP3 regulatory axis to control alveolar macrophage pyroptosis in acute lung injury.Acta biochimica et biophysica Sinica · 2024Article
- Plumbagin inhibits fungal growth, HMGB1/LOX-1 pathway and inflammatory factors inFrontiers in microbiology · 2024Article
- Prevention of severe lung immunopathology associated with influenza infection through adeno-associated virus vector administration.Laboratory animal research · 2023Article
- Article
- Review
- Anti-inflammatory effect and antihepatoma mechanism of carrimycin.World journal of gastroenterology · 2023Article
- Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023Review
- Venous thromboembolism in viral diseases: A comprehensive literature review.Health science reports · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlveolar macrophages are sentinels of the airways that must exhibit immune restraint to innocuous antigens but elicit a robust inflammatory response to pathogenic threats. How distinction between these dichotomous functions is controlled is poorly defined.Neutrophils are the first responders to infection, and we hypothesised that they may free alveolar macrophages from their hyporesponsive state, promoting their activation. Activation of the inflammasome and interleukin (IL)-1β release is a key early inflammatory event that must be tightly regulated. Thus, the role of neutrophils in defining inflammasome activation in the alveolar macrophage was assessed.
methodsMice were infected with the X31 strain of influenza virus and the role of neutrophils in alveolar macrophage activation established through administration of a neutrophil-depleting (1A8) antibody.
resultsInfluenza elicited a robust IL-1β release that correlated (r=0.6849; p<0.001) with neutrophil infiltrate and was ablated by neutrophil depletion. Alveolar macrophages were shown to be the prominent source of IL-1β during influenza infection, and virus triggered the expression of Nod-like receptor protein 3 (NLRP3) inflammasome and pro-IL-1β in these cells. However, subsequent activation of the inflammasome complex and release of mature IL-1β from alveolar macrophages were critically dependent on the provision of a secondary signal, in the form of antimicrobial peptide mCRAMP, from infiltrating neutrophils.
conclusionsNeutrophils are critical for the activation of the NLRP3 inflammasome in alveolar macrophages during respiratory viral infection. Accordingly, we rationalise that neutrophils are recruited to the lung to confront a viable pathogenic threat and subsequently commit alveolar macrophages to a pro-inflammatory phenotype to combat infection.
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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.