ArticleAmerican journal of respiratory cell and molecular biology2012
Apolipoprotein A-I attenuates ovalbumin-induced neutrophilic airway inflammation via a granulocyte colony-stimulating factor-dependent mechanism.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Comorbidities, Associated Diseases, and Risk Assessment in COVID-19-A Systematic Review.International journal of clinical practice · 2022Pooled it
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- Modulation of the NF-κB signaling pathway by the combined strategy of tocilizumab and dexamethasone for asthma therapy.Respiratory research · 2026Article
- Apolipoprotein A-I: a non-negligible marker in hypertriglyceridemia-induced acute pancreatitis.European journal of medical research · 2025Article
- Human neutrophils are a cellular source of apolipoprotein A-I.Journal of leukocyte biology · 2025Article
- Causal Relationships Between Blood Lipid Levels and Chronic Obstructive Pulmonary Disease: A Mendelian Randomization Analysis.International journal of chronic obstructive pulmonary disease · 2025Article
- Correlation between neutrophil-to-high-density lipoprotein cholesterol ratio (NHR) and adverse prognosis in patients who achieve complete recanalization after thrombectomy for acute large vessel occlusion stroke.Frontiers in neurology · 2025Article
- Neutrophil-related immune-inflammatory biomarkers influence the early progression of medial medullary infarction.Frontiers in neurology · 2025Article
- Association between high-density lipoprotein-related inflammation index and periodontitis: insights from NHANES 2009-2014.Lipids in health and disease · 2024Article
- Neutrophil Heterogeneity Is Modified during Acute Lung Inflammation in Apoa1-/- Mice.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Serum proteomics identifies novel diagnostic biomarkers for asthma in preschool children.Journal of thoracic disease · 2024Article
- Anti-inflammatory mechanism of Apolipoprotein A-I.Frontiers in immunology · 2024Review
- A computational approach for the identification of key genes and biological pathways of chronic lung diseases: a systems biology approach.BMC medical genomics · 2023Article
- Scavenger receptor BI attenuates oxidized phospholipid-induced pulmonary inflammation.Toxicology and applied pharmacology · 2023Article
- Sterols and immune mechanisms in asthma.The Journal of allergy and clinical immunology · 2023Review
- Sterols in asthma.Trends in immunology · 2022Review
- HDL and Therapy.Advances in experimental medicine and biology · 2022Article
- Scavenger Receptor BI Attenuates IL-17A-Dependent Neutrophilic Inflammation in Asthma.American journal of respiratory cell and molecular biology · 2021Article
- Scavenger Hunt: SR-B1, Adrenal Insufficiency, IL-17A, and Neutrophilic Airway Inflammation in Asthma.American journal of respiratory cell and molecular biology · 2021Article
- Current Understanding of the Immunomodulatory Activities of High-Density Lipoproteins.Biomedicines · 2021Review
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Apolipoprotein A-I (apoA-I) is a key component of high-density lipoproteins that mediates reverse cholesterol transport from cells and reduces vascular inflammation. We investigated whether endogenous apoA-I modulates ovalbumin (OVA)-induced airway inflammation in mice. We found that apoA-I expression was significantly reduced in the lungs of OVA-challenged, compared with saline-challenged, wild-type (WT) mice. Next, to investigate the role of endogenous apoA-I in the pathogenesis of OVA-induced airway inflammation, WT and apoA-I(-/-) mice were sensitized by intraperitoneal injections of OVA and aluminum hydroxide, followed by multiple nasal OVA challenges for 4 weeks. OVA-challenged apoA-I(-/-) mice exhibited a phenotype of increased airway neutrophils compared with WT mice, which could be rescued by an administration of a 5A apoA-I mimetic peptide. Multiple pathways promoted neutrophilic inflammation in OVA-challenged apoA-I(-/-) mice, including the up-regulated expression of (1) proinflammatory cytokines (IL-17A and TNF-α), (2) CXC chemokines (CXCL5), (3) vascular adhesion molecules (i.e., vascular cell adhesion molecule-1), and (4) granulocyte colony-stimulating factors (G-CSF). Because concentrations of G-CSF in bronchoalveolar lavage fluid (BALF) were markedly increased in OVA-challenged apoA-I(-/-) mice, we hypothesized that enhanced G-CSF expression may represent the predominant pathway mediating increased neutrophilic inflammation. This was confirmed by the intranasal administration of a neutralizing anti-G-CSF antibody, which significantly reduced BALF neutrophilia by 72% in OVA-challenged apoA-I(-/-) mice, compared with mice that received a control antibody. We conclude that endogenous apoA-I negatively regulates OVA-induced neutrophilic airway inflammation, primarily via a G-CSF-dependent mechanism. Furthermore, these findings suggest that apoA-I may play an important role in modulating the severity of neutrophilic airway inflammation in asthma.
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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.