Abstract
Background
Ankylosing spondylitis (AS) is a progressive, disabling joint disease that affects millions worldwide. There is a lack of useful disease model to conduct comprehensive mechanistic studies. Non-human primate model is a potential spontaneous model for ankylosing spondylitis (AS).
Methods
A group of cynomolgus monkeys with abnormal joints and abnormal movements were screened out from about 20,000 cynomolgus monkeys primarily. A 2-years follow-up study of this group of cynomolgus monkeys having joint lesions reported of spinal stiffness was performed by conducting hematological testing, radiographic examination, family aggregation analysis, pathological analysis and genetic testing.
Results
These diseased animals suffered from spontaneous AS with clinical features recapitulating human AS disease progression. The spontaneous incidence rate and the onset age of AS in monkeys similar to epidemiological features of AS patients. The disease progression in disease monkeys have shown bone erosion, osteophyte formation and “Bamboo-like” change. ESR, CRP IL-17, TNF-α and VEGF levels significantly increase in AS monkeys comparing with normal monkeys. Several features similar to AS patients, including cartilage destruction, cartilage ossification, chondroid metaplasia and bone formation were shown in AS monkeys pathological examination results. Both the serum bone resorption and bone formation biomarkers of AS monkeys were significantly reduce. In our current SNP sequencing results, loci that similar to AS-relative SNPs in human genome have not yet been found.
Conclusions
The study offers a promising non-human primate model for spontaneous ankylosing spondylitis which may serve as an excellent substitute for its pre-clinical research.
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