The role of microbiota and oxidative stress axis and the impact of intravenous immunoglobulin in systemic lupus erythematosus

Abstract

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by widespread inflammation affecting various organs. This review discusses the role of oxidative stress and gut microbiota in the pathogenesis of SLE and evaluates the therapeutic potential of intravenous immunoglobulins (IVIg). Oxidative stress contributes to SLE by causing impairment in the function of mitochondria, resulting in reactive oxygen species production, which triggers autoantigenicity and proinflammatory cytokines. Gut microbiota also plays a significant role in SLE. Dysbiosis has been associated to disease's onset and progression. Moreover, dysbiosis exacerbates SLE symptoms and influences systemic immunity, leading to a breakdown in bacterial tolerance and an increase in inflammatory responses. High-dose IVIg has emerged as a promising treatment for refractory cases of SLE. The beneficial effects of IVIg are partly due to its antioxidant property, reducing oxidative stress markers and modulating the immune responses. Additionally, IVIg can normalize the gut flora, as demonstrated in a case of severe intestinal pseudo-obstruction. In summary, both oxidative stress and dysregulation of microbiota are pivotal in the pathogenesis of SLE. The use of IVIg may improve the disease's outcome. Future research should be directed to elucidating the precise mechanisms by which oxidative stress and microbiota are linked with autoimmunity in SLE in developing targeted therapies.

Keywords: Dysbiosis; Intravenous immunoglobulin; Mitochondria; Oxidative stress; Reactive oxygen species; Redox; Respiratory chain; Systemic lupus erythematosus.