Oxidative stress and immune complexes: Pathogenic mechanisms in pristane induced murine model of lupus.

Systemic lupus erythematosus is a systemic autoimmune inflammatory disease with a broad spectrum of clinical presentations. Mouse models play an indispensible role in understanding the disease pathology and for developing new therapeutics. This study investigated the effect of pristane administration on female BALB/c mice. The various manifestations of lupus replicated in this mouse model were analysed and their relevance to human disease was assessed. Pristane injection replicates the two prime manifestations of lupus i.e. oxidative stress and inflammation. An increase in oxidative stress was determined by the decreasing anti-oxidants, increasing ROS and lipid peroxidation. Inflammatory cytokines (IL-6 and TNF-α) also increased in the plasma. The deteriorating organ functions after pristane administration were evident histopathologically. An increase in inflammatory cells, necrosis, oil vacuoles and pigment cells were marked in kidney, liver, lungs and spleen, whereas skin did not manifest any alteration. Liver function (bilirubin, SGPT) and kidney function (creatinine and proteinuria) tests were also altered. Pristane injection caused the generation of anti-nuclear antibodies, which were apparent from the different immunofluorescence patterns observed. Immune deposits were evident in all the vital organs stating the similarity this model holds with lupus patients. Replicating various manifestations of human lupus disorder, pristane induced mouse model of lupus serves as an appropriate model to study lupus complications and in the development of novel therapeutics for disease management.