Influence of Corynebacterium parvum-per on disease progression in the NZB/W model of systemic lupus erythematosus

Abstract

Murine models of systemic lupus erythematosus (SLE) exhibit some, but not all, of the characteristics of human disease. Disease progression in the animal models is regulated by autoantibodies, genetics and inflammatory processes. In the present study, the influence of the pyridine extract residue of Corynebacterium parvum Type I (CP-PER) on disease progression in the NZB/W model of SLE was investigated. CP-PER is known to activate the reticuloendothelial (RE) system of mice and can alter a number of host reponses. Injection of NZB/W females with CP-PER at 10 weeks of age, prior to the onset of overt disease, led to a transient activation of the RE system which then appeared to return to levels observed in untreated animals. Sera from treated and untreated animals were analyzed for anti-nuclear antibodies, and anti-ssDNA antibodies. The most prominant change in the treated animals was an increase in the titer of anti-ssDNA. On average, animals in the early treatment group also lived somewhat longer than those in the untreated control group. Treatment of animals with CP-PER at 6 months of age, when the disease was evident, again led to transient RES activation and an altered autoantibody profile. Animals treated with CP-PER at 6 months of age exhibited a slightly accelerated death rate when compared with the untreated controls. These results indicate that bacterial response modifiers such as C. parvum-PER, which contains primarily the RES activating activity of C. parvum, can alter disease progression in the NZB/W model.