ArticleMucosal immunology2015
Activation of C3a receptor is required in cigarette smoke-mediated emphysema.
Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Identification of HIF1A as a therapeutic target during SARS-CoV-2-associated lung injury.JCI insight · 2025Trial
- A Single Cell Atlas of the COPD Lung Identifies Inflammatory Reprogramming in Fibroblasts.International journal of chronic obstructive pulmonary disease · 2026Article
- Larval Ascariasis Triggers Unresolved Anemia, Persistent Inflammation, and Chronic Pulmonary Disease after Single and Reinfection in a Dose-Dependent Manner in Mice.ACS infectious diseases · 2025Article
- Smoking status and vascular risk factors as predictors of disability in AQP4-NMOSD and MOGAD.Multiple sclerosis (Houndmills, Basingstoke, England) · 2025Article
- Validation of Systemic Complement Signatures in the Progression of Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2024Article
- Article
- Environmental tobacco smoke exposure exaggerates bleomycin-induced collagen overexpression during pulmonary fibrogenesis.Journal of inflammation (London, England) · 2024Article
- The persistent inflammation in COPD: is autoimmunity the core mechanism?European respiratory review : an official journal of the European Respiratory Society · 2024Review
- The effect of smoking on MRI lesion resolution in NMOSD-AQP4 and MOGAD.Multiple sclerosis (Houndmills, Basingstoke, England) · 2023Article
- A blood and bronchoalveolar lavage protein signature of rapid FEVScientific reports · 2023Article
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- SARS-CoV-2 Infection: Host Response, Immunity, and Therapeutic Targets.Inflammation · 2022Review
- Activation of C3 and C5 May Be Involved in the Inflammatory Progression of PCM and GM.Inflammation · 2022Article
- Transient Ascaris suum larval migration induces intractable chronic pulmonary disease and anemia in mice.PLoS neglected tropical diseases · 2021Article
- Targeting Complement C3a Receptor to Improve Outcome After Ischemic Brain Injury.Neurochemical research · 2021Review
- Review
- Interaction Between the Complement System and Infectious Agents - A Potential Mechanistic Link to Neurodegeneration and Dementia.Frontiers in cellular neuroscience · 2021Review
- Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System.Journal of visualized experiments : JoVE · 2020Article
- Article
- Adenosine at the Interphase of Hypoxia and Inflammation in Lung Injury.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Exposure to cigarette smoke can initiate sterile inflammatory responses in the lung and activate myeloid dendritic cells (mDCs) that induce differentiation of T helper type 1 (Th1) and Th17 cells in the emphysematous lungs. Consumption of complement proteins increases in acute inflammation, but the contribution of complement protein 3 (C3) to chronic cigarette smoke-induced immune responses in the lung is not clear. Here, we show that following chronic exposure to cigarette smoke, C3-deficient (C3(-/-)) mice develop less emphysema and have fewer CD11b(+)CD11c(+) mDCs infiltrating the lungs as compared with wild-type mice. Proteolytic cleavage of C3 by neutrophil elastase releases C3a, which in turn increases the expression of its receptor (C3aR) on lung mDCs. Mice deficient in the C3aR (C3ar(-/-)) partially phenocopy the attenuated responses to chronic smoke observed in C3(-/-) mice. Consistent with a role for C3 in emphysema, C3 and its active fragments are deposited on the lung tissue of smokers with emphysema, and smoke-exposed mice. Together, these findings suggest a critical role for C3a through autocrine/paracrine induction of C3aR in the pathogenesis of cigarette smoke-induced sterile inflammation and provide new therapeutic targets for the treatment of emphysema.
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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.