ArticleAmerican journal of respiratory and critical care medicine2013
Serum amyloid A promotes lung neutrophilia by increasing IL-17A levels in the mucosa and γδ T cells.
Article in American journal of respiratory and critical care medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 67 citations in OpenAlex.
- An airway epithelial IL-17A response signature identifies a steroid-unresponsive COPD patient subgroup.The Journal of clinical investigation · 2019Trial
- Trial
- Serum amyloid A: multifaceted roles in inflammation and cellular interactions.Immunologic research · 2025Review
- The Role ofBiomolecules · 2025Review
- ALX/FPR2 Contributes to Serum Amyloid A-Induced Lung Neutrophil Recruitment Following Acute Ozone Exposure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Serum Amyloid A: A Double-Edged Sword in Health and Disease.International journal of molecular sciences · 2025Review
- Combined Inflammatory Markers for Predicting Acute Exacerbations in Chronic Obstructive Pulmonary Disease With Respiratory Failure.Journal of inflammation research · 2025Article
- Article
- Achieving quantitative reproducibility in label-free multisite DIA experiments through multirun alignment.Communications biology · 2023Article
- Serum Amyloid A in Stable Patients with Chronic Obstructive Pulmonary Disease Does Not Reflect the Clinical Course of the Disease.International journal of molecular sciences · 2023Article
- Serum amyloid A as a biomarker for immunoglobulin resistance in Kawasaki disease.Annals of medicine · 2023Article
- Acute-serum amyloid A and A-SAA-derived peptides as formyl peptide receptor (FPR) 2 ligands.Frontiers in endocrinology · 2023Review
- Mechanisms of Corticosteroid Resistance in Type 17 Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Mesenchymal Stem Cells and Formyl Peptide Receptor 2 Activity in Hyperoxia-Induced Lung Injury in Newborn Mice.International journal of molecular sciences · 2022Article
- Serum amyloid A 1 induces suppressive neutrophils through the Toll-like receptor 2-mediated signaling pathway to promote progression of breast cancer.Cancer science · 2022Article
- Effects of serum amyloid protein A on influenza A virus replication and viral interactions with neutrophils.Journal of leukocyte biology · 2021Article
- Article
- Inflammatory Endotype-associated Airway Microbiome in Chronic Obstructive Pulmonary Disease Clinical Stability and Exacerbations: A Multicohort Longitudinal Analysis.American journal of respiratory and critical care medicine · 2021Article
- Emerging and multifaceted role of neutrophils in lung cancer.Translational lung cancer research · 2021Review
- Accelerated atherosclerosis caused by serum amyloid A response in lungs of ApoEFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
rationaleNeutrophilic inflammation is an important pathologic feature of chronic obstructive pulmonary disease (COPD) and infectious exacerbations of COPD. Serum amyloid A (SAA) promotes neutrophilic inflammation by its interaction with lung mucosal ALX/FPR2 receptors. However, little is known about how this endogenous mediator regulates IL-17A immunity.
objectivesTo determine whether SAA causes neutrophilic inflammation by IL-17A-dependent mechanisms.
methodsThe relationship between SAA and neutrophils was investigated in lung sections from patients with COPD and a chronic mouse model of SAA exposure. A neutralizing antibody to IL-17A was used to block SAA responses in vivo, and a cell-sorting strategy was used to identify cellular sources. MEASUREMENTS AND MAIN
resultsSAA mRNA expression was positively associated with tissue neutrophils in COPD (P < 0.05). SAA predominately promoted expression of the TH17 polarizing cytokine IL-6, which was opposed by 15-epi-lipoxin A4, a counter-regulatory mediator, and ALX/FPR2 ligand. SAA-induced inflammation was markedly reduced by a neutralizing antibody to IL-17A in vivo. Cellular sources of IL-17A induced by SAA include CD4(+) T cells, γδ T cells, and an Epcam(+)CD45(-) population enriched for epithelial cells. SAA promotes expression of IL-17A in γδ T cells and this innate cell proportionally expressed higher levels of IL-17A transcript than CD4(+) T cells or epithelial cells.
conclusionsThe SAA-IL-17A axis represents an important innate defense network that may underlie persistent neutrophilic airway inflammation in COPD and modulating the ALX/FPR2 receptor represents a novel approach to targeting aberrant IL-17A-mediated lung immunity.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.