Auricular chondritis in NOD.DQ8.Aβo (Ag7–/–) transgenic mice resembles human relapsing polychondritis

Taneja, Veena; Griffiths, Marie; Behrens, Marshall D.; Luthra, Harvinder S.; David, Chella S.

doi:10.1172/jci17450

Cited by 12 publications

(10 citation statements)

References 43 publications

(44 reference statements)

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“…It is also known that anti-collagen antibodies, mainly Type II, can be seen during an acute RP episode; these antibodies are probably the result of the liberation of inflammatory cytokines such as TNF α , IL1, and IL6 [14, 15]. The main clinical manifestation of RP is uni- or bilateral auricular chondritis, as seen in our patient.…”

Section: Discussionsupporting

confidence: 62%

Relapsing Polychondritis in a Patient with Ankylosing Spondylitis Using Etanercept

Azevedo

Galli

Kleinfelder

et al. 2014

Case Reports in Rheumatology

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Relapsing polychondritis (RP) is an autoimmune disease characterized by recurrent episodes of inflammation and progressive destruction of cartilaginous tissues, especially of the ears, nose, joints, and tracheobronchial tree. Its etiology is not well understood, but some studies have linked its pathophysiology with autoimmune disease and autoantibody production. We described a case of a 46-year-old male patient with ankylosing spondylitis who developed RP after the use of etanercept. Few similar cases have been described in the literature. However, they show a possible association between the use of biological inhibitors of tumor necrosis factor (anti-TNFα), which potentially produces autoantibodies, and the development of RP. The treatment was based on data in the literature and included the cessation of biological therapy and the addition of corticosteroids with substantial improvement.

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Section: Discussionsupporting

confidence: 62%

Relapsing Polychondritis in a Patient with Ankylosing Spondylitis Using Etanercept

Azevedo

Galli

Kleinfelder

et al. 2014

Case Reports in Rheumatology

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“…Interestingly, seven out of 97 RP patients showed concomitant presence of anti-matrilin-1 and anti-COMP antibodies, suggesting that immunization against COMP may be a consequence of the matrilin-1 mediated process of cartilage destruction. Experimental studies in murine models confirmed that immunization with extracellular matrix proteins can result in the development of a chondritis closely resembling the clinical picture observed in human RP patients [ 21 , 22 ]. The role of cell-mediated immune response in the pathophysiology of RP is supported by several data.…”

Section: Pathogenesismentioning

confidence: 74%

Relapsing Polychondritis: An Updated Review

et al. 2018

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Relapsing polychondritis is an immune-mediated systemic disease characterized by recurrent episodes of inflammation of cartilaginous and proteoglycan-rich tissues, resulting in progressive anatomical deformation and functional impairment of the involved structures. Auricular and nasal chondritis and/or polyarthritis represent the most common clinical features, but potentially all types of cartilage may be involved. Because of the pleomorphic nature of the disease, with non-specific symptoms at the onset, the diagnosis of relapsing polychondritis is often delayed. In this review article we provide a comprehensive look into clinical presentation, laboratory and instrumental investigations, diagnostic criteria, and therapeutic options.

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“…To evaluate the T-cell response to Collinsella -primed dendritic cells (DCs), 10 days post-immunization, splenic CD4 T cells sorted from CII-primed DQ8 mice (200 μg of CII emulsified 1:1 in complete Freund's adjuvant (CFA) were cultured in vitro in the presence or absence of CII (50 μg/ml) and DCs (pre-cultured with bacteria or supernatant of the bacterial culture). T-cell proliferation was measured by routine 3 H-thymidine incorporation [ 23 ]. All experiments were done two to three times for reproducibility.…”

Section: Methodsmentioning

confidence: 99%

An expansion of rare lineage intestinal microbes characterizes rheumatoid arthritis

et al. 2016

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BackgroundThe adaptive immune response in rheumatoid arthritis (RA) is influenced by an interaction between host genetics and environment, particularly the host microbiome. Association of the gut microbiota with various diseases has been reported, though the specific components of the microbiota that affect the host response leading to disease remain unknown. However, there is limited information on the role of gut microbiota in RA. In this study we aimed to define a microbial and metabolite profile that could predict disease status. In addition, we aimed to generate a humanized model of arthritis to confirm the RA-associated microbe.MethodsTo identify an RA biomarker profile, the 16S ribosomal DNA of fecal samples from RA patients, first-degree relatives (to rule out environment/background as confounding factors), and random healthy non-RA controls were sequenced. Analysis of metabolites and their association with specific taxa was performed to investigate a potential mechanistic link. The role of an RA-associated microbe was confirmed using a human epithelial cell line and a humanized mouse model of arthritis.ResultsPatients with RA exhibited decreased gut microbial diversity compared with controls, which correlated with disease duration and autoantibody levels. A taxon-level analysis suggested an expansion of rare taxa, Actinobacteria, with a decrease in abundant taxa in patients with RA compared with controls. Prediction models based on the random forests algorithm suggested that three genera, Collinsella, Eggerthella, and Faecalibacterium, segregated with RA. The abundance of Collinsella correlated strongly with high levels of alpha-aminoadipic acid and asparagine as well as production of the proinflammatory cytokine IL-17A. A role for Collinsella in altering gut permeability and disease severity was confirmed in experimental arthritis.ConclusionsThese observations suggest dysbiosis in RA patients resulting from the abundance of certain rare bacterial lineages. A correlation between the intestinal microbiota and metabolic signatures could determine a predictive profile for disease causation and progression.Electronic supplementary materialThe online version of this article (doi:10.1186/s13073-016-0299-7) contains supplementary material, which is available to authorized users.

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Auricular chondritis in NOD.DQ8.Aβo (Ag7–/–) transgenic mice resembles human relapsing polychondritis

Cited by 12 publications

References 43 publications

Relapsing Polychondritis in a Patient with Ankylosing Spondylitis Using Etanercept

Relapsing Polychondritis in a Patient with Ankylosing Spondylitis Using Etanercept

Relapsing Polychondritis: An Updated Review

An expansion of rare lineage intestinal microbes characterizes rheumatoid arthritis

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