Abstract
Gut microbiota has a strong influence on the onset and development of systemic lupus erythematosus (SLE), and several studies have demonstrated the effectiveness of microbiota-derived butyrate to ameliorate SLE. However, the roles of butyrate on gut microbiota in SLE are not understood. Using MRL/lpr lupus-prone mice, we examined gut microbiota profiles after butyrate treatment by 16S rRNA sequencing. Alterations in intestinal microbiome in mice with lupus-like disease were mainly characterized by a reduction in microbial diversity, with an increased abundance of Bacteroidetes and a decrease of Firmicutes. Treatment of lupus-prone mice with butyrate resulted in increased abundance of Firmicutes (P = 0.003), Clostridia (P = 0.005), Clostridiales (P = 0.005), Lachnospiraceae (P = 0.009), Ruminococcaceae (P = 0.021), Peptostreptococcaceae (P = 0.021), Ruminiclostridium (P = 0.016), Oscillibacter (P = 0.048), Romboutsia (P = 0.025), Lachnoclostridium (P = 0.012), Coprococcus (P = 0.015), Ruminococcus (P = 0.011), Clostridium leptum (P < 0.05), and Dorea_spp. (P = 0.019), and a reduced proportion of Bacteroidetes (P = 0.004), Bacteroidia (P = 0.004), and Bacteroidales (P = 0.004). Further, butyrate supplementation could ameliorate kidney damage. Overall, this study suggests that gut microbiota alterations occur in MRL/lpr lupus-prone mice following treatment with butyrate. Butyrate supplementation ameliorated gut microbiota dysbiosis. These findings support the use of butyrate and butyrate-producing bacteria as potential treatments for SLE.
Highlights
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disorder that damages multiple organs, including the kidneys, joints, skin, lung, heart, and brain [1]
MRL/lpr mice were gavaged with sodium butyrate or phosphate-buffered saline (PBS) starting from 8 weeks until 16 weeks of age
One mouse in the MRL/lpr model group was found dead at week 11, while no deaths occurred in the BALB/c group and butyrate-treated MRL/lpr group
Summary
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disorder that damages multiple organs, including the kidneys, joints, skin, lung, heart, and brain [1]. The pathogenesis of lupus is unclear, genetic predisposition as well as hormonal and environmental factors are involved. There is no cure, and treatment relies mainly on immunosuppressants. The symptoms are effectively managed with immunosuppressants, the side effects of these therapeutic drugs are concerning. Patients undergoing prolonged immunosuppression are more likely to experience higher infection rates and more serious infections. There is an urgent need to explore the pathophysiological mechanisms of SLE and develop new treatment strategies
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