Interleukin 1 enhances the development of spontaneous arthritis in MRL/lpr mice.
We previously reported that treatments with human recombinant interleukin-1 beta (rIL-1 beta) in DBA/1 mice which were suboptimally immunized with native chick type II collagen (NcII) markedly accelerated the onset of collagen-induced arthritis (CIA). In the present study, we further characterized this IL-1-mediated enhancement of murine arthritis by examining the in vivo effects of rIL-1 beta in another arthritis model, namely, the spontaneous arthritis of the MRL/lpr mouse strain. The results of these studies demonstrated that IL-1 treatments also enhanced the onset and progression of the spontaneous arthritic disease in MRL/lpr mice. A substantial proportion of the IL-1-treated MRL/lpr mice that were between 3 and 3.5 months of age exhibited swelling in either the hind or front paws. Moreover, histopathologic studies demonstrated the presence of striking alterations within the various joints of these IL-1-treated MRL/lpr mice. Such abnormalities were not detected in the non-IL-1-treated, age-matched MRL/lpr mice. Therefore, as in the experimentally induced disease of CIA, IL-1 may also be capable of contributing to the pathogenesis of the spontaneous arthritis of MRL/lpr mice.
Hom
J T
JT
Department of Connective Tissue and Monoclonal Antibody Research, Lilly Research Laboratories, Indianapolis, Indiana 46285.
Cole
H
H
Bendele
A M
AM
D000818:Animals; D001168:Arthritis / Q000209:etiology*; D001169:Arthritis, Experimental / Q000209:etiology* / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D007375:Interleukin-1 / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains
D007375:Interleukin-1