Cargando…
Gut Microbiota Aberration in Patients of Systemic Sclerosis and Bleomycin-Induced Mice Model
Systemic sclerosis (SSc) is an immune-mediated systemic autoimmune disease with unknown etiology, which has high morbidity and mortality. Current treatments to dispose of this disorder are limited. And there are still no ideal animal models that can fully replicate the four basic pathophysiological...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8193929/ https://www.ncbi.nlm.nih.gov/pubmed/34123867 http://dx.doi.org/10.3389/fcimb.2021.647201 |
Sumario: | Systemic sclerosis (SSc) is an immune-mediated systemic autoimmune disease with unknown etiology, which has high morbidity and mortality. Current treatments to dispose of this disorder are limited. And there are still no ideal animal models that can fully replicate the four basic pathophysiological features of SSc, including vascular lesions, fibrosis, inflammation, and autoimmunity, let alone animal models specifically designed to study gastrointestinal lesions. It’s essential to seek and establish appropriate animal models to explore the role of gut microbiota in the pathogenesis of SSc. In this study, we found similar gut microbiota aberration in patients of SSc and bleomycin (BLM)-induced mice model through 16S rRNA gene sequencing. In terms of phylum-level differences, the relative abundance of Bacteroidetes was significantly decreased and Firmicutes increased in the SSc patients and the mice. Notably, the genera of Lactobacillus, commonly used as a probiotic additive, was also elevated in SSc patients and BLM mice, which was consistent with a few of studies. Therefore, the model can likely mimic the pathological changes of gut microbiota in patients with SSc, which may offer an important potential platform for the in-depth understanding of gut microbiota aberration in patients with SSc and to devise potential disease-modifying treatments. |
---|