ArticleInvestigative ophthalmology & visual science2009
NOD1 expression in the eye and functional contribution to IL-1beta-dependent ocular inflammation in mice.
Article in Investigative ophthalmology & visual science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- NOD1 deficiency ameliorates the progression of diabetic retinopathy by modulating bone marrow-retina crosstalk.Stem cell research & therapy · 2024Article
- The Pathogenesis of Staphylococcus aureus Eye Infections.Pathogens (Basel, Switzerland) · 2018Review
- New insights into Nod-like receptors (NLRs) in liver diseases.International journal of physiology, pathophysiology and pharmacology · 2018Review
- Efficacy of the nucleotide-binding oligomerzation domain 1 inhibitor Nodinhibit-1 on corneal alkali burns in rats.International journal of ophthalmology · 2015Article
- Investigation of the peptidoglycan sensing molecule, PGLYRP-2, in murine inflammatory uveitis.The British journal of ophthalmology · 2013Article
- Muller glia in retinal innate immunity: a perspective on their roles in endophthalmitis.Critical reviews in immunology · 2013Review
- Roles of NOD1 (NLRC1) and NOD2 (NLRC2) in innate immunity and inflammatory diseases.Bioscience reports · 2012Review
- Interferon-γ regulates discordant mechanisms of uveitis versus joint and axial disease in a murine model resembling spondylarthritis.Arthritis and rheumatism · 2012Article
- The NLRP3 inflammasome is active but not essential in endotoxin-induced uveitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012Article
- Interplay between innate and adaptive immunity in the development of non-infectious uveitis.Progress in retinal and eye research · 2012Review
- Neutralization of IL-17 ameliorates uveitis but damages photoreceptors in a murine model of spondyloarthritis.Arthritis research & therapy · 2012Article
- Retinal astrocytes pretreated with NOD2 and TLR2 ligands activate uveitogenic T cells.PloS one · 2012Article
- Investigation of the differential potentials of TLR agonists to elicit uveitis in mice.Journal of leukocyte biology · 2011Article
- Contrasting ocular effects of local versus systemic endotoxin.Investigative ophthalmology & visual science · 2011Article
- NLRs in immune privileged sites.Current opinion in pharmacology · 2011Review
- Discovery and characterization of 2-aminobenzimidazole derivatives as selective NOD1 inhibitors.Chemistry & biology · 2011Article
- NOD2 deficiency results in increased susceptibility to peptidoglycan-induced uveitis in mice.Investigative ophthalmology & visual science · 2011Article
- Inflammasomes and their activation.Critical reviews in immunology · 2010Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
purposeNOD1 plays an important role in host defense and recognizes the minimal component of bacterial cell walls, meso-diaminopimelic acid (iE-DAP). Polymorphisms in NOD1 are associated with autoinflammatory diseases characterized by uveitis such as Crohn's disease and sarcoidosis. NOD1 is homologous to NOD2, which is responsible for an autosomal dominant form of uveitis. Nonetheless, the role of NOD1 in intraocular inflammation has not been explored. The induction of uveitis by iE-DAP in mice and the potential contribution of interleukin (IL)-1beta were investigated.
methodsBALB/c mice or mice deficient in caspase-1 or IL-1R1 and their congenic controls were injected intravitreally with iE-DAP or saline. The time course, dose response, and contribution of IL-1beta to ocular inflammation were quantified by intravital video microscopy, histology, and immunohistochemistry. NOD1 and IL-1beta were measured in eye tissue by immunoblotting and ELISA.
resultsNOD1 protein is expressed in the eye and promotes ocular inflammation in a dose- and time-dependent fashion. The authors previously defined the role of IL-1beta in NOD2 uveitis and tested whether NOD1 and NOD2 used similar mechanisms. Treatment with iE-DAP significantly increased IL-1beta, which was caspase-1 dependent. However, in contrast to NOD2, caspase-1 and IL-1R1 were essential mediators of iE-DAP-induced uveitis, suggesting that NOD1 and NOD2 induce ocular inflammation by distinct mechanisms involving IL-1beta.
conclusionsThese findings demonstrate that NOD1 is expressed within the eye and that its activation results in uveitis in an IL-1beta-dependent mechanism. Characterizing the differences between NOD1 and NOD2 responses may provide insight into the pathogenesis of uveitis.
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