Role of reactive intermediates in the immunopathogenesis of the pristane-induced Balb/c model of lupus

Pristane-induced lupus in Balb/c mice represents an environmentally induced lupus model which is widely used for unravelling the mystery of the pathogenesis of the disease. An intraperitoneal innate immune reaction to pristane is primarily accountable for the development of the systemic lupus erythematosus-like disease in the model. In this study, reactive oxygen species (ROS) and nitric oxide (NO) levels were assessed (as a measure of chronic inflammation) in the peritoneum of the Balb/c model of SLE-like disease 6 months after a single intraperitoneal injection of pristane. Levels of ROS in peritoneal macrophages were significantly enhanced (mean fluorescence value ± SD: 648 ± 100.9) in pristane-treated mice (PT) as compared with control mice (mean fluorescence value ± SD: 79 ± 7.8) treated with phosphate buffer saline (PBST). An immunofluorescence study reveal the localization of ROS within nuclei, suggesting oxidative damage. Similarly, levels of NO were also markedly raised in PT mice (34.71 µmol/l ± 8.48) as compared with PBST mice (1.36 nmol/l ± 0.14). These new findings lead to speculation about the role of reactive intermediates in the development of disease. This study proposes that the sustained production of reactive intermediates during chronic intraperitoneal inflammation might reduce antioxidant defences and lead to a condition of oxidative stress, which might further be responsible for this autoimmune condition.


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