ArticleAmerican journal of respiratory cell and molecular biology2009
Leukotriene B4 release from mast cells in IgE-mediated airway hyperresponsiveness and inflammation.
Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- Leukotriene B4 regulates T cell recognition and control of MCMV in mucosal tissues.Mucosal immunology · 2025Article
- Differential expression of eicosanoid pathways after whole blood stimulation in asthma patients.The World Allergy Organization journal · 2025Article
- Article
- Blockade of the BLT1-LTBScientific reports · 2022Article
- Machine-learning algorithms for asthma, COPD, and lung cancer risk assessment using circulating microbial extracellular vesicle data and their application to assess dietary effects.Experimental & molecular medicine · 2022Article
- An inhibitor of leukotriene-AProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Montelukast induces beneficial behavioral outcomes and reduces inflammation in male and female rats.Frontiers in immunology · 2022Article
- Connections between Immune-Derived Mediators and Sensory Nerves for Itch Sensation.International journal of molecular sciences · 2021Review
- The Kinetics of Lymphatic Dysfunction and Leukocyte Expansion in the Draining Lymph Node during LTBInternational journal of molecular sciences · 2021Article
- Roles of mast cells in rheumatoid arthritis.The Korean journal of internal medicine · 2020Review
- CD8European respiratory review : an official journal of the European Respiratory Society · 2019Review
- Mast Cells and Their Progenitors in Allergic Asthma.Frontiers in immunology · 2019Review
- Ozone Exerts Cytoprotective and Anti-Inflammatory Effects in Cardiomyocytes and Skin Fibroblasts after Incubation with Doxorubicin.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Mast Cell-Dependent CD8Cancer immunology research · 2018Article
- Leukotrienes and sex: strange bedfellows?The Journal of clinical investigation · 2017Article
- Spectrum of T-lymphocyte activities regulating allergic lung inflammation.Immunological reviews · 2017Review
- 1,25D3 prevents CD8(+)Tc2 skewing and asthma development through VDR binding changes to the Cyp11a1 promoter.Nature communications · 2016Article
- The sphingosine-1-phosphate/sphingosine-1-phosphate receptor 2 axis regulates early airway T-cell infiltration in murine mast cell-dependent acute allergic responses.The Journal of allergy and clinical immunology · 2015Article
- Stepwise epigenetic and phenotypic alterations poise CD8+ T cells to mediate airway hyperresponsiveness and inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Requirement for chemokine receptor 5 in the development of allergen-induced airway hyperresponsiveness and inflammation.American journal of respiratory cell and molecular biology · 2011Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Previous studies have shown that leukotriene B4 (LTB4), a proinflammatory lipid mediator, is linked to the development of airway hyperresponsiveness through the accumulation of IL-13-producing CD8+ T cells, which express a high affinity receptor for LTB4, BLT1 (Miyahara et al., Am J Respir Crit Care Med 2005;172:161-167; J Immunol 2005;174:4979-4984). By using leukotriene A4 hydrolase-deficient (LTA4H-/-) mice, which fail to synthesize LTB4, we determined the role of this lipid mediator in allergen-induced airway responses. Two approaches were used. In the first, LTA4H-/- mice and wild-type (LTA4H+/+) mice were systemically sensitized and challenged via the airways to ovalbumin. In the second, mice were passively sensitized with anti-ovalbumin IgE and exposed to ovalbumin via the airways. Mast cells were generated from bone marrow of LTA4H+/+ mice or LTA4H-/- mice. After active sensitization and challenge, LTA4H-/- mice showed significantly lower airway hyperresponsiveness compared with LTA4H+/+ mice, and eosinophil numbers and IL-13 levels in the bronchoalveoloar lavage of LTA4H-/- mice were also significantly lower. LTA4H-/- mice also showed decreased airway reactivity after passive sensitization and challenge. After LTA4H+/+ mast cell transfer, LTA4H-/- mice showed increased airway reactivity after passive sensitization and challenge, but not after systemic sensitization and challenge. These data confirm the important role for LTB4 in the development of altered airway responses and suggest that LTB4 secretion from mast cells is critical to eliciting increased airway reactivity after passive sensitization with allergen-specific IgE.
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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.