Characterization of a spontaneously occurring arthritis in male DBA/1 mice

Nordling, Cecilia; Karlsson‐Parra, Alex; Jansson, Liselotte; Holmdahl, Rikard; Klareskog, Lars

doi:10.1002/art.1780350619

Cited by 57 publications

(37 citation statements)

References 13 publications

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“…Because no serological analysis was done at this time, any comment on these data would be speculative. It has been reported that DBA/1 mice may develop arthritis spontaneously (11,39). The possible effect of dietary CLA during the relapse period could be similar to what has been reported in the lupus model of autoimmunity.…”

Section: Discussionsupporting

confidence: 76%

A mechanistic approach to understanding conjugated linoleic acid's role in inflammation using murine models of rheumatoid arthritis

Bütz¹,

Li²,

Huebner³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: Discussionsupporting

confidence: 76%

A mechanistic approach to understanding conjugated linoleic acid's role in inflammation using murine models of rheumatoid arthritis

Bütz¹,

Li²,

Huebner³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Additionally, the kinetics of arthritis development can vary from experiment to experiment as evidenced by the comparison of the incidence rate in the two independent experiments shown in Figure 2. Older male DBA/1 mice (44 months of age) should be avoided for CIA experiments as there is some evidence that these mice develop a spontaneous arthritis 26,27 . These patterns are similar in all of the arthritis-susceptible strains, with the possible exception of the C57BL/6 (B6) mouse.…”

Section: Anticipated Resultsmentioning

confidence: 99%

Collagen-induced arthritis

2007

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The collagen-induced arthritis (CIA) mouse model is the most commonly studied autoimmune model of rheumatoid arthritis. Autoimmune arthritis is induced in this model by immunization with an emulsion of complete Freund's adjuvant and type II collagen (CII). This protocol describes the steps necessary for acquisition, handling and preparation of CII, as well as selection of mouse strains, proper immunization technique and evaluation of the arthritis incidence and severity. Typically, the first signs of arthritis appear in this model 21-28 days after immunization, and identification of the arthritic limbs is not difficult. Using the protocol described, the investigator should be able to reproducibly induce a high incidence of CIA in various strains of genetically susceptible mice as well as learn how to critically evaluate the pathology of the disease. The total time for the preparation of reagents and the immunization of ten mice is about 1.5 h.

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“…However, only male DBA/1 mice over the age of 4 months spontaneously develop arthropathy in their ankles or lower extremities. The lesions are characterized pathologically by abnormal proliferation of bone and cartilage, which is referred to as enthesopathy, without significant immunologic abnormalities (11,12). The arthropathy of DBA/1 mice histopathologically resembles, in part, ankylosing spondylitis or diffuse idiopathic skeletal hyperostosis (13) in humans, but it never develops in the joints of the spine.…”

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confidence: 99%

Accelerating effect of an MRL gene locus on the severity and onset of arthropathy in DBA/1 mice

Oishi¹,

Miyazaki²,

Mizuki³

et al. 2005

Arthritis & Rheumatism

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Objective. To analyze the influence of the genetic background of an arthritis-prone strain of mice, MRL, on the spontaneous development of arthropathy in DBA/1 mice, which histopathologically resembles enthesopathy in humans, and to clarify the strain-specific gene loci and their interactions that confer susceptibility to arthropathy.Methods. MRL, DBA/1, (MRL ؋ DBA/1)F 1 , and (MRL ؋ DBA/1)F 2 intercross mice were prepared, and the severity and onset of arthropathy of the ankle joints in individual mice were quantified (0-3 and 0-5 scale, respectively). A genome-wide scan of 271 male F 2 intercross mice with polymorphic microsatellite markers was performed.Results. Only male DBA/1, (MRL ؋ DBA/1)F 1 , and (MRL ؋ DBA/1)F 2 mice developed arthropathy. The macroscopic and histopathologic findings of arthropathy in the F 2 mice were similar to those in the parental DBA/1 mice, but the onset was significantly earlier. In the quantitative trait locus analysis of male F 2 mice, 1 susceptibility locus for both the severity and early onset of the disease in the region of an MRL allele, Amd1, was located at marker D10Mit259 (map position 40.0 cM), which was common to 1 of the sialadenitis susceptibility loci in MRL mice, Asm1. Another susceptibility locus for the severity and early onset of arthropathy in the region of a DBA allele, Amd2, was located at D3Mit46 (29.5 cM). These loci manifested an additive effect on the development of arthropathy.Conclusion. Arthropathy in DBA/1 mice is under the control of an allelic combination of gene loci, one of which is common to the locus for sialadenitis in MRL/ MpJ-lpr/lpr mice.

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Characterization of a spontaneously occurring arthritis in male DBA/1 mice

Cited by 57 publications

References 13 publications

A mechanistic approach to understanding conjugated linoleic acid's role in inflammation using murine models of rheumatoid arthritis

A mechanistic approach to understanding conjugated linoleic acid's role in inflammation using murine models of rheumatoid arthritis

Collagen-induced arthritis

Accelerating effect of an MRL gene locus on the severity and onset of arthropathy in DBA/1 mice

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