POLYARTHRITIS AND PERIOSTITIS INDUCED BY ESCHERICHIA-COLI - LIPOPOLYSACCHARIDE INJECTION IN YOUNG MALE HAMSTERS

Citation
E. Gruys et al., POLYARTHRITIS AND PERIOSTITIS INDUCED BY ESCHERICHIA-COLI - LIPOPOLYSACCHARIDE INJECTION IN YOUNG MALE HAMSTERS, Journal of rheumatology, 25(4), 1998, pp. 748-752
Citations number
27
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
0315162X
Volume
25
Issue
4
Year of publication
1998
Pages
748 - 752
Database
ISI
SICI code
0315-162X(1998)25:4<748:PAPIBE>2.0.ZU;2-Z
Abstract
Objective, To describe the clinicopathological manifestations of lipop olysaccharide (LPS) induced arthritis in the hamster and to compare it s time of onset, duration, and severity with other forms of experiment ally induced arthritis. Methods, A preparation containing 30 mu g LPS from Escherichia coli was injected subcutaneously for 5 to 21 days int o young male hamsters (Mesocricetus auratus). Arthritis was quantified by measuring soft tissue swelling of affected joints with calipers. A fter decalcification, paraffin sections were cut and stained with hema toxylin and eosin, Giemsa, and azan. Acute phase reactant apolipoprote in serum amyloid A (apoSAA) levels were determined by ELISA. Results, Symmetrical polyarthritis developed within 3 days and persisted for 14 -21 days, provided the hamsters received daily LPS injections. Most pr ominent were lesions in the carpal-metacarpal joints of the front legs and in the tarsal-metatarsal joints of the hind legs. Animals in whom LPS injections were discontinued after 4 or 7 days recovered complete ly. Histological findings of exudative synovitis, periarticular soft t issue swelling, and juxtaarticular periostitis were associated with a sharp rise in serum titers of apoSAA. Conclusion, The unusually rapid onset of arthritis and periostitis in this experimental animal model s uggests that its systemic manifestations were not mediated by a classi cal immune response, and may represent an ''innate'' response of targe ted cells within the synovial membrane and periosteum to bacterial cel l wall endotoxins.