ArticleThe American journal of pathology1995
Role of interleukin 1 in antigen-induced exacerbations of murine arthritis.
Article in The American journal of pathology, 1995. 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, 75 citations in OpenAlex.
- Cytokine Autoantibodies Alter Gene Expression Profiles of Healthy Donors.European journal of immunology · 2025Article
- Transthyretin deposition promotes progression of osteoarthritis.Aging cell · 2017Article
- Suppression and resolution of autoimmune arthritis by rhesus θ-defensin-1, an immunomodulatory macrocyclic peptide.PloS one · 2017Article
- Article
- Identification of two new arthritis severity loci that regulate levels of autoantibodies, interleukin-1β, and joint damage in pristane- and collagen-induced arthritis.Arthritis and rheumatism · 2012Article
- JNK-1 deficiency limits macrophage-mediated antigen-induced arthritis.Arthritis and rheumatism · 2011Article
- Evaluating intra-articular drug delivery for the treatment of osteoarthritis in a rat model.Tissue engineering. Part B, Reviews · 2010Review
- Tumor necrosis factor-alpha in temporomandibular joint synovial fluid predicts treatment effects on pain by intra-articular glucocorticoid treatment.Mediators of inflammation · 2006Article
- Blocking of interleukin-17 during reactivation of experimental arthritis prevents joint inflammation and bone erosion by decreasing RANKL and interleukin-1.The American journal of pathology · 2005Article
- Disease-modifying therapies for osteoarthritis : current status.Drugs & aging · 2005Review
- An inflammation-inducible adenoviral expression system for local treatment of the arthritic joint.Gene therapy · 2004Article
- Anti-interleukin 1alpha autoantibodies.Annals of the rheumatic diseases · 2002Article
- The development of clinical signs of rheumatoid synovial inflammation is associated with increased synthesis of the chemokine CXCL8 (interleukin-8).Arthritis research · 2001Article
- Anti-cytokine therapy in chronic destructive arthritis.Arthritis research · 2001Review
- Arguments for interleukin 1 as a target in chronic arthritis.Annals of the rheumatic diseases · 2000Review
- Role of tumour necrosis factor alpha in experimental arthritis: separate activity of interleukin 1beta in chronicity and cartilage destruction.Annals of the rheumatic diseases · 1999Review
- Increased vulnerability of postarthritic cartilage to a second arthritic insult: accelerated MMP activity in a flare up of arthritis.Annals of the rheumatic diseases · 1999Article
- Joint inflammation and cartilage destruction may occur uncoupled.Springer seminars in immunopathology · 1998Review
- Interleukin-6 reduces cartilage destruction during experimental arthritis. A study in interleukin-6-deficient mice.The American journal of pathology · 1997Article
- Cytokine and nitric oxide production in the acute phase of bacterial cell wall-induced arthritis.Inflammation · 1997Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism underlying the chronic and intermittent course of rheumatoid arthritis is not elucidated. In the present study, the role of interleukin 1 (IL-1) was investigated in exacerbations of antigen-induced arthritis in mice. A flare-up of smoldering inflammation (weeks 3 to 4 of antigen-induced arthritis) was inducible by injection of a small amount of methylated bovine serum albumin into the hypersensitive knee joint. Immunohistochemistry showed IL-1 expression in the synovial lining layer and in focal areas of the inflamed synovium during the flare-up. IL-1 was also measured in 1-hour culture supernatant of synovial tissue taken during the flare-up by a bioassay. The expression of both immunoreactive and bioactive IL-1 in the hypersensitive joint peaked around 6 hours after antigen (2 micrograms of methylated bovine serum albumin) injection and declined thereafter. Antigen rechallenge induced an acute joint swelling of the arthritic joint but not in the naive joint of the sensitized mouse, yet synovia of both joints produced IL-1 after antigen injection. Remarkably, a single intravenous injection of rabbit anti-IL-1 alpha and -beta antibodies 1 hour before antigen rechallenge neutralized IL-1 in the joint. Anti-IL-1 treatment significantly reduced the antigen-induced joint swelling (30 to 40%) but did not affect the profound influx of polymorphonuclear cells in the onset of the exacerbation. However, a profound relief of the inflammation (synovitis) was obtained by IL-1 blockade on day 4 of the exacerbation. Chondrocyte proteoglycan synthesis was markedly suppressed in the antigen-challenged naive knee joints suggesting that this was a direct IL-1 effect as the inflammation was insignificant. Anti-IL-1 treatment was able to maintain chondrocyte proteoglycan synthesis in the antigen-rechallenged joint, which was highly suppressed in the control group. Furthermore, the enhanced proteoglycan breakdown in the antigen-rechallenged joints was significantly decreased in the anti-IL-1 group. We concluded that IL-1 is an important mediator in exacerbations of murine arthritis, and amelioration of cartilage pathology was obtained with anti-IL-1 antibody treatment.
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7856731PMC1870767W2159141726What OpenQuestion holds
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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.