ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Joint tissues amplify inflammation and alter their invasive behavior via leukotriene B4 in experimental inflammatory arthritis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Metabolic changes in fibroblast-like synoviocytes in rheumatoid arthritis: state of the art review.Frontiers in immunology · 2024Review
- The Role of G Protein-Coupled Receptor Kinase 6 Regulation in Inflammation and Pain.International journal of molecular sciences · 2022Review
- Toxoplasma gondii Infection Decreases Intestinal 5-Lipoxygenase Expression, while Exogenous LTBInfection and immunity · 2022Article
- Fatty Acids and Oxylipins in Osteoarthritis and Rheumatoid Arthritis-a Complex Field with Significant Potential for Future Treatments.Current rheumatology reports · 2021Review
- Differential Metabolome in Rheumatoid Arthritis: a Brief Perspective.Current rheumatology reports · 2021Review
- Lipid Metabolism Profiles in Rheumatic Diseases.Frontiers in pharmacology · 2021Review
- Phenolic acid phenethylesters and their corresponding ketones: Inhibition of 5-lipoxygenase and stability in human blood and HepaRG cells.Pharmacology research & perspectives · 2019Article
- Identification of a novel autoantibody against self-vimentin specific in secondary Sjögren's syndrome.Arthritis research & therapy · 2018Article
- Host Lipid Mediators in Leprosy: The Hypothesized Contributions to Pathogenesis.Frontiers in immunology · 2018Review
- Fibroblast-like synoviocyte metabolism in the pathogenesis of rheumatoid arthritis.Arthritis research & therapy · 2017Review
- An evaluation of the protective role of vitamin C in reactive oxygen species-induced hepatotoxicity due to hexavalent chromium in vitro and in vivo.Journal of occupational medicine and toxicology (London, England) · 2017Article
- Persisting eicosanoid pathways in rheumatic diseases.Nature reviews. Rheumatology · 2014Review
- The interrelationship between leukotriene B4 and leukotriene-A4-hydrolase in collagen/adjuvant-induced arthritis in rats.BioMed research international · 2014Article
- Role of neutrophils in systemic autoimmune diseases.Arthritis research & therapy · 2013Review
- 5-lipoxygenase deficiency reduces acetaminophen-induced hepatotoxicity and lethality.BioMed research international · 2013Article
- Lipid-cytokine-chemokine cascades orchestrate leukocyte recruitment in inflammation.Journal of leukocyte biology · 2012Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Mechanisms by which mesenchymal-derived tissue lineages participate in amplifying and perpetuating synovial inflammation in arthritis have been relatively underinvestigated and are therefore poorly understood. Elucidating these processes is likely to provide new insights into the pathogenesis of multiple diseases. Leukotriene B(4) (LTB(4)) is a potent proinflammatory lipid mediator that initiates and amplifies synovial inflammation in the K/BxN model of arthritis. We sought to elucidate mechanisms by which mesenchymal-derived fibroblast-like synoviocytes (FLSs) perpetuate synovial inflammation. We focused on the abilities of FLSs to contribute to LTB(4) synthesis and to respond to LTB(4) within the joint. Using a series of bone marrow chimeras generated from 5-lipoxygenase(-/-) and leukotriene A(4) (LTA(4)) hydrolase(-/-) mice, we demonstrate that FLSs generate sufficient levels of LTB(4) production through transcellular metabolism in K/BxN serum-induced arthritis to drive inflammatory arthritis. FLSs-which comprise the predominant lineage populating the synovial lining-are competent to metabolize exogenous LTA(4) into LTB(4) ex vivo. Stimulation of FLSs with TNF increased their capacity to generate LTB(4) 3-fold without inducing the expression of LTA(4) hydrolase protein. Moreover, LTB(4) (acting via LTB(4) receptor 1) was found to modulate the migratory and invasive activity of FLSs in vitro and also promote joint erosion by pannus tissue in vivo. Our results identify novel roles for FLSs and LTB(4) in joints, placing LTB(4) regulation of FLS biology at the center of a previously unrecognized amplification loop for synovial inflammation and tissue pathology.
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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.