ArticleAmerican journal of respiratory and critical care medicine2008
Airway lipoxin A4 generation and lipoxin A4 receptor expression are decreased in severe asthma.
Article in American journal of respiratory and critical care medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
What it found
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Who cites it
99 citing papers in PubMed, 251 citations in OpenAlex.
- Mechanisms and therapeutic strategies of asthma: from bench to bedside.Signal transduction and targeted therapy · 2026Review
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 2026Review
- Integrated pro-resolving mechanisms: a new dimension for optimizing anti-inflammatory therapy in asthma - a review of impaired inflammation resolution in airway remodeling.Frontiers in immunology · 2026Review
- Single-Cell Insights Into Macrophage Subtypes in Pulmonary Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Resolution Pharmacology: State-of-the-art and therapeutic landscape.Pharmacological reviews · 2025Review
- Evaluation of the Effects of Lipoxin A4 and Resolvin D1 on the Severity of Transient Tachypnea of the Newborn: A Prospective Study.Children (Basel, Switzerland) · 2025Article
- Reprogramming inflammation: Mechanisms and therapeutic targeting of eicosanoids and pro-resolving mediators.European journal of pharmacology · 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
- Linking Lipid Metabolism and Immune Function: New Insights into Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- RvD1 improves resident alveolar macrophage self-renewal via the ALX/MAPK14/S100A8/A9 pathway in acute respiratory distress syndrome.Journal of advanced research · 2025Article
- Single-cell analysis reveals alterations in cellular composition and cell-cell communication associated with airway inflammation and remodeling in asthma.Respiratory research · 2024Article
- Natural killer cells in the lung: potential role in asthma and virus-induced exacerbation?European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Mast cells contribute to the resolution of allergic inflammation by releasing resolvin D1.Pharmacological research · 2023Article
- The role of oxylipins in NSAID-exacerbated respiratory disease (N-ERD).Advances in pharmacology (San Diego, Calif.) · 2023Article
- Exogenous Lipoxin A4 attenuates IL4-induced Mucin Expression in Human Airway Epithelial Cells.International journal of medical sciences · 2023Article
- Article
- Formylpeptide receptor 2: Nomenclature, structure, signalling and translational perspectives: IUPHAR review 35.British journal of pharmacology · 2022Review
- Arachidonate 15-lipoxygenase type B: Regulation, function, and its role in pathophysiology.Frontiers in pharmacology · 2022Review
- The Role of Defective Epithelial Barriers in Allergic Lung Disease and Asthma Development.Journal of asthma and allergy · 2022Review
- Placental Expression and Relative Role of Anti-inflammatory Annexin A1 and Animal Lectin Galectin-3 in the Pathogenesis of Preeclampsia.Indian journal of clinical biochemistry : IJCB · 2022Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 10 institutions in 2 countries.
Funding
Abstract
rationaleAirway inflammation is common in severe asthma despite antiinflammatory therapy with corticosteroids. Lipoxin A(4) (LXA(4)) is an arachidonic acid-derived mediator that serves as an agonist for resolution of inflammation.
objectivesAirway levels of LXA(4), as well as the expression of lipoxin biosynthetic genes and receptors, in severe asthma.
methodsSamples of bronchoalveolar lavage fluid were obtained from subjects with asthma and levels of LXA(4) and related eicosanoids were measured. Expression of lipoxin biosynthetic genes was determined in whole blood, bronchoalveolar lavage cells, and endobronchial biopsies by quantitative polymerase chain reaction, and leukocyte LXA(4) receptors were monitored by flow cytometry. MEASUREMENTS AND MAIN
resultsIndividuals with severe asthma had significantly less LXA(4) in bronchoalveolar lavage fluids (11.2 +/- 2.1 pg/ml) than did subjects with nonsevere asthma (150.1 +/- 38.5 pg/ml; P < 0.05). In contrast, levels of cysteinyl leukotrienes were increased in both asthma cohorts compared with healthy individuals. In severe asthma, 15-lipoxygenase-1 mean expression was decreased fivefold in bronchoalveolar lavage cells. In contrast, 15-lipoxgenase-1 was increased threefold in endobronchial biopsies, but expression of both 5-lipoxygenase and 15-lipoxygenase-2 in these samples was decreased. Cyclooxygenase-2 expression was decreased in all anatomic compartments sampled in severe asthma. Moreover, LXA(4) receptor gene and protein expression were significantly decreased in severe asthma peripheral blood granulocytes.
conclusionsMechanisms underlying pathological airway responses in severe asthma include lipoxin underproduction with decreased expression of lipoxin biosynthetic enzymes and receptors. Together, these results indicate that severe asthma is characterized, in part, by defective lipoxin counterregulatory signaling circuits.
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