Pathogenesis of Antigen-Induced Arthritis

Me, Steinberg; Cr, McCrae; Ld, Cohen; Hr, Schumacher

doi:10.1097/00003086-197311000-00031

Cited by 19 publications

(5 citation statements)

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“…Antigen‐induced arthritis (AIA), originally described by Dumonde and Glynn [1], can be induced by immunization of rabbits, rats or mice with an antigen such as fibrin and ovalbumin (OVA) [2] followed by the intraarticular injection of the relevant antigen. There are histological similarities between AIA and human rheumatoid arthritis, including hyperplasia of synovium forming pannus, a massive infiltration of inflammatory cells including neutrophils and mononuclear cells [3, 4]. Both cellular and humoral immune responses are involved in AIA [3, 5].…”

Section: Introductionmentioning

confidence: 99%

Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

et al. 2005

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We examined whether oral administration of lipopolysaccharide (LPS) from Escherichia coli reactivated antigen-induced arthritis (AIA) in mice that is one of models of human rheumatoid arthritis. To induce AIA, mice were immunized by subcutaneous injection of ovalbumin (OVA) emulsified with complete Freund's adjuvant into the base of the tail (day 0) followed by intraarticular injection of OVA on day 21. To investigate the ability of LPS to reactivate AIA, varying doses of LPS were p.o. administered 48 h after the challenge injection. The results showed that administration of LPS was followed by reactivation of AIA in a dose-related fashion. The reactivation of AIA by LPS was associated with increases in interferon-g, interleukin-1b and tumour necrosis factor-a. Polymyxin B sulfate given immediately before administration of LPS suppressed the reactivation of AIA. These findings suggest that LPS from intestinal bacteria may play a role in the reactivation of joint inflammation in which immune responses to pathogenic antigens are involved.

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Section: Introductionmentioning

confidence: 99%

Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

et al. 2005

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“…Dis Chest 56: [19][20][21][22][23]1969 29. Rutherford RB, Rhodes BA, Wagner NH: The distribution of extremity blood flow before and after vagectomy in a patient with hypertrophic pulmonary osteoarthropathy.…”

mentioning

confidence: 99%

Articular manifestations of hypertrophic pulmonary osteoarthropathy in bronchogenic carcinoma. A clinical and pathologic study

Schumacher

1976

Arthritis & Rheumatism

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Eight patients with bronchogenic carcinoma presented with painful joint effusions as part of the syndrome of hypertrophic osteoarthropathy. Elevated sedimentation rates and symptomatic relief with aspirin were common, but synovial fluids all had leukocyte counts less than 500/mm3. Synovial microvascular injury was found in all patients, and electron-dense deposits in synovial vessel walls were identified in 5 cases. These vascular deposits suggest a role for circulating materials in pathogenesis.Painful swelling around knees, ankles, wrists, and occasionally fingers may be the presenting manifestation of hypertrophic pulmonary osteoarthropathy (HPO) but can easily be mistaken clinically for rheumatoid arthritis (1,2). Clubbing may be subtle but is rarely absent. Because HPO may be an important early clue to the diagnosis of bronchogenic carcinoma and other pulmonary mass lesions, this report describes 8 cases and emphasizes some characteristics of the arthropathy that should help raise the possibility of a diagnosis of HPO. ~_ _ _ _From the Veterans Administration Hospital and the University of Pennsylvania.

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“…All cell types, except the PMNs, maintained relatively constant or increasing levels in the synovial tissue up to the last time point investigated, which was 2 months. Figure 3 does not indicate the other changes observed in the synovium, such as increased vascularity, lining layer cell hypertrophy, and hyperplasia, increased fibrosis, and the occurrence of foci of lymphocytes and plasma cells characteristic of this synovitis model (4)(5)(6). Figure 4A depicts a histologic section of synovial tissue from a knee 6 hours after challenge with 0.5 mg of BSA.…”

Section: R Esu Lts 8-glucuronidase Correlation With Pmns In Jointmentioning

confidence: 94%

Effects of antiinflammatory agents on the acute response of immune synovitis in rabbits

Goldlust

Rich²,

Harrity³

1977

Arthritis & Rheumatism

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Immune synovitis in rabbits was investigated as a potential in vivo model for evaluating new antiinflammatory agents. Antigen-induced increases in knee width as well as P-glucuronidase and acid phosphatase activities in exudates were observed. Histologically, polymorphonuclear leukocytes appeared within hours in synovial tissues and reached maximum infiltration at about 24 hours. Subsequently, mononuclear cells, including plasma cells, appeared. The 6-hour Arthus-like phase of synovitis can be depressed by some antiinflammatory agents, colchicine and steroids being particularly effective. It is suggested that this model can be utilized to define potentially more effective antiinflammatory drugs.

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Pathogenesis of Antigen-Induced Arthritis

Cited by 19 publications

References 0 publications

Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

Articular manifestations of hypertrophic pulmonary osteoarthropathy in bronchogenic carcinoma. A clinical and pathologic study

Effects of antiinflammatory agents on the acute response of immune synovitis in rabbits

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