ArticleThe American journal of pathology2003
Deficiency of NADPH oxidase components p47phox and gp91phox caused granulomatous synovitis and increased connective tissue destruction in experimental arthritis models.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 96 citations in OpenAlex.
- The type 1 and type 3 immune responses underlying the tissue inflammation associated with NOX2 deficiency.Frontiers in immunology · 2026Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Nox, Nox, Are You There? The Role of NADPH Oxidases in the Peripheral Nervous System.Antioxidants & redox signaling · 2022Review
- Biological Effects of β-Glucans on Osteoclastogenesis.Molecules (Basel, Switzerland) · 2021Review
- Mice Deficient in NOX2 Display Severe Thymic Atrophy, Lymphopenia, and Reduced Lymphopoiesis in a Zymosan-Induced Model of Systemic Inflammation.Inflammation · 2021Article
- Skeletal muscle redox signaling in rheumatoid arthritis.Clinical science (London, England : 1979) · 2020Review
- Decorin knockdown affects the gene expression profile of adhesion, growth and extracellular matrix metabolism in C-28/I2 chondrocytes.PloS one · 2020Article
- Experimental lupus is aggravated in mouse strains with impaired induction of neutrophil extracellular traps.JCI insight · 2017Article
- Articular inflammation induced by an enzymatically-inactive Lys49 phospholipase AThe journal of venomous animals and toxins including tropical diseases · 2017Article
- Immunometabolism and autoimmunity.Immunology and cell biology · 2016Review
- Impact of reactive oxygen species (ROS) on the control of parasite loads and inflammation in Leishmania amazonensis infection.Parasites & vectors · 2016Article
- Reactive oxygen species deficiency induces autoimmunity with type 1 interferon signature.Antioxidants & redox signaling · 2014Article
- Neutrophil activation during acetaminophen hepatotoxicity and repair in mice and humans.Toxicology and applied pharmacology · 2014Article
- Burkholderia cenocepacia J2315 escapes to the cytosol and actively subverts autophagy in human macrophages.Cellular microbiology · 2014Article
- NADPH oxidase limits lipopolysaccharide-induced lung inflammation and injury in mice through reduction-oxidation regulation of NF-κB activity.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Identification of a region in p47phox/NCF1 crucial for phagocytic NADPH oxidase (NOX2) activation.Journal of leukocyte biology · 2013Article
- NOX2 protects against prolonged inflammation, lung injury, and mortality following systemic insults.Journal of innate immunity · 2013Article
- New tricks from an old dog: mitochondrial redox signaling in cellular inflammation.Seminars in immunology · 2012Review
- Decreased STAT5 phosphorylation and GATA-3 expression in NOX2-deficient T cells: role in T helper development.European journal of immunology · 2012Article
- Regulation of innate immunity by NADPH oxidase.Free radical biology & medicine · 2012Review
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Recent studies indicated that the nicotinamide dinucleotide phosphate oxidase (NADPH) oxidase-derived oxygen radicals plays a deleterious role in arthritis. To study this in more detail, gonarthritis was induced in NADPH oxidase-deficient mice. Mice received an intraarticular injection of either zymosan, to elicit an irritant-induced inflammation, or poly-L-lysine coupled lysozyme, to evoke an immune-complex mediated inflammation in passively immunized mice. In contrast to wild-type mice, arthritis elicited in both p47phox(-/-) and gp91(-/-) mice showed more severe joint inflammation, which developed into a granulomatous synovitis. Treatment with either Zileuton or cobra venom factor showed that the chemokines LTB4 and complement C3 were not the driving force behind the aggravated inflammation in these mice. Arthritic NADPH oxidase-deficient mice showed irreversible cartilage damage as judged by the enhanced aggrecan VDIPEN expression, and chondrocyte death. Furthermore, only in the absence of NADPH oxidase-derived oxygen radicals, the arthritic joints showed osteoclast-like cells, tartrate-resistant acid phosphatase (TRAP)-positive/multinucleated cells, extensive bone erosion, and osteolysis. The enhanced synovial gene expression of tumor necrosis factor-alpha, interleukin-1alpha, matrix metalloproteinase (MMP)-3, MMP-9 and receptor activator of NF-kappaB ligand (RANKL) might contribute to the aggravated arthritis in the NADPH oxidase-deficient mice. This showed that the involvement of NADPH oxidase in arthritis is probably far more complex and that oxygen radicals might also be important in controlling disease severity, and reducing joint inflammation and connective tissue damage.
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