Interleukin 1 enhances the development of spontaneous arthritis in MRL/lpr mice

• Published in: Clinical immunology and immunopathology Vol. 55; no. 1; p. 109
• Main Authors: Hom, J T, Cole, H, Bendele, A M
• Format: Journal Article
• Language: English
• Published: United States 01-04-1990
• Subjects: Animals; Arthritis - etiology; Arthritis, Experimental - etiology; Arthritis, Experimental - pathology; Disease Models, Animal; Female; Interleukin-1 - pharmacology; Male; Mice; Mice, Inbred Strains
• ISSN: 0090-1229
• DOI: 10.1016/0090-1229(90)90072-X

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.