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Probiotic Limosilactobacillus reuteri DSM 17938 Changes Foxp3 Deficiency-Induced Dyslipidemia and Chronic Hepatitis
Erini Nessim Kostandy1, Ji Ho Suh2, Xiangjun Tian3
1Department of Pediatrics, Division of Gastroenterology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Abstract:
The probiotic Limosilactobacillus reuteri DSM 17938 produces anti-inflammatory effects in scurfy (SF) mice, a model characterized by immune dysregulation, polyendocrinopathy, enteropathy, and X-linked inheritance (called IPEX syndrome in humans), caused by regulatory T cell (Treg) deficiency and is due to a Foxp3 gene mutation. Considering the pivotal role of lipids in autoimmune inflammatory processes, we investigated alterations in the relative abundance of lipid profiles in SF mice (± treatment with DSM 17938) compared to normal WT mice. We also examined the correlation between plasma lipids and gut microbiota and circulating inflammatory markers. We noted a significant upregulation of plasma lipids associated with autoimmune disease in SF mice, many of which were downregulated by DSM 17938. The upregulated lipids in SF mice demonstrated a significant correlation with gut bacteria known to be implicated in the pathogenesis of various autoimmune diseases. Chronic hepatitis in SF livers responded to DSM 17938 treatment with a reduction in hepatic inflammation. Altered gene expression associated with lipid metabolism and the positive correlation between lipids and inflammatory cytokines together suggest that autoimmunity leads to dyslipidemia with impaired fatty acid oxidation in SF mice. Probiotics are presumed to contribute to the reduction of lipids by reducing inflammatory pathways.
Insights
The probiotic Limosilactobacillus reuteri DSM 17938 reduced autoimmune-associated lipid changes in scurfy mice. This suggests probiotics may help manage autoimmune diseases by modulating lipid profiles and inflammation.
Area of Science:
- Immunology
- Microbiology
- Metabolomics
Background:
- Scurfy (SF) mice exhibit immune dysregulation, similar to human IPEX syndrome, due to regulatory T cell (Treg) deficiency.
- Lipids play a crucial role in autoimmune inflammatory processes.
- Limosilactobacillus reuteri DSM 17938 demonstrates anti-inflammatory effects.
Purpose of the Study:
- To investigate lipid profile alterations in SF mice with and without DSM 17938 treatment.
- To examine correlations between plasma lipids, gut microbiota, and inflammatory markers.
- To understand the impact of autoimmunity on lipid metabolism.
Main Methods:
- Lipidomic analysis of plasma from SF mice (treated and untreated) and wild-type (WT) mice.
- Correlation analysis between lipid profiles, gut microbiota composition, and inflammatory markers.
- Assessment of hepatic inflammation and gene expression related to lipid metabolism.
Main Results:
- SF mice showed significant upregulation of plasma lipids linked to autoimmune disease, many of which were normalized by DSM 17938 treatment.
- Upregulated lipids in SF mice correlated with specific gut bacteria implicated in autoimmune pathogenesis.
- DSM 17938 treatment reduced hepatic inflammation in SF mice, alongside altered gene expression in lipid metabolism.
Conclusions:
- Autoimmunity in SF mice leads to dyslipidemia and impaired fatty acid oxidation.
- Limosilactobacillus reuteri DSM 17938 may ameliorate autoimmune conditions by downregulating pro-autoimmune lipids.
- Probiotics show potential in managing autoimmune diseases through lipid metabolism modulation and inflammation reduction.
