ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
FABP4 regulates eosinophil recruitment and activation in allergic airway inflammation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Discerning asthma endotypes through comorbidity mapping.Nature communications · 2022Pooled it
- Autoallergy in chronic rhinosinusitis and its clinical relevance.The World Allergy Organization journal · 2026Article
- Leukocyte-Based Inflammatory Profiles Across Dyslipidemia Phenotypes: Patterns of Eosinophil-Related Indices.Medicina (Kaunas, Lithuania) · 2025Article
- Constructing a 3D co-cultureMaterials today. Bio · 2025Article
- FABP4 as a therapeutic host target controlling SARS-CoV-2 infection.EMBO molecular medicine · 2025Article
- First Trimester Placental Biomarkers for Pregnancy Outcomes.International journal of molecular sciences · 2024Review
- Pathophysiological Insight into Fatty Acid-Binding Protein-4: Multifaced Roles in Reproduction, Pregnancy, and Offspring Health.International journal of molecular sciences · 2023Review
- Desmoglein 2 Functions as a Receptor for Fatty Acid Binding Protein 4 in Breast Cancer Epithelial Cells.Molecular cancer research : MCR · 2023Article
- Starch intake, amylase gene copy number variation, plasma proteins, and risk of cardiovascular disease and mortality.BMC medicine · 2023Article
- FABP3, FABP4, and heart rate variability among patients with chronic schizophrenia.Frontiers in endocrinology · 2023Article
- FABP4-mediated lipid droplet formation in Streptococcus uberis-infected macrophages supports host defence.Veterinary research · 2022Article
- FABP4 secreted by M1-polarized macrophages promotes synovitis and angiogenesis to exacerbate rheumatoid arthritis.Bone research · 2022Article
- Cigarette smoke extract-mediated FABP4 upregulation suppresses viability and induces apoptosis, inflammation and oxidative stress of bronchial epithelial cells by activating p38 MAPK/MK2 signaling pathway.Journal of inflammation (London, England) · 2022Article
- Yanghe Pingchuan Granules Alleviate Airway Inflammation in Bronchial Asthma and Inhibit Pyroptosis by Blocking the TLR4/NF-Mediators of inflammation · 2022Article
- FABP4 knockdown suppresses inflammation, apoptosis and extracellular matrix degradation in IL-1β-induced chondrocytes by activating PPARγ to regulate the NF-κB signaling pathway.Molecular medicine reports · 2021Article
- FABP5 as a possible biomarker in atopic march: FABP5-induced Th17 polarization, both in mouse model and human samples.EBioMedicine · 2020Article
- Regulation of Eosinophil Recruitment and Allergic Airway Inflammation by Tropomyosin Receptor Kinase A.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Reduced airway levels of fatty-acid binding protein 4 in COPD: relationship with airway infection and disease severity.Respiratory research · 2020Article
- Fatty acid-binding proteins: functional understanding and diagnostic implications.Current opinion in clinical nutrition and metabolic care · 2019Review
- FABP4 contributes to renal interstitial fibrosis via mediating inflammation and lipid metabolism.Cell death & disease · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Fatty acid binding protein 4 (FABP4), a member of a family of lipid-binding proteins, is known to play a role in inflammation by virtue of its ability to regulate intracellular events such as lipid fluxes and signaling. Studies have indicated a proinflammatory role for FABP4 in allergic asthma although its expression and function in eosinophils, the predominant inflammatory cells recruited to allergic airways, were not investigated. We examined expression of FABP4 in murine eosinophils and its role in regulating cell recruitment in vitro as well as in cockroach antigen (CRA)-induced allergic airway inflammation. CRA exposure led to airway recruitment of FABP4-expressing inflammatory cells, specifically eosinophils, in wild-type (WT) mice. FABP4 expression in eosinophils was induced by TNF-α as well as IL-4 and IL-13. FABP4-deficient eosinophils exhibited markedly decreased cell spreading/formation of leading edges on vascular cell adhesion molecule-1 and significantly decreased adhesion to intercellular adhesion molecule-1 associated with reduced β2-integrin expression relative to WT cells. Furthermore, FABP4-deficient eosinophils exhibited decreased migration, F-actin polymerization, calcium flux, and ERK(1/2) phosphorylation in response to eotaxin-1. In vivo, CRA-challenged FABP4-deficient mice exhibited attenuated eosinophilia and significantly reduced airway inflammation (improved airway reactivity, lower IL-5, IL-13, TNF-α, and cysteinyl leukotriene C4 levels, decreased airway structural changes) compared with WT mice. In conclusion, expression of FABP4 in eosinophils is induced during conditions of inflammation and plays a proinflammatory role in the development of allergic asthma by promoting eosinophil adhesion and migration and contributing to the development of various aspects of airway inflammation.
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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 Socratic graph.