Treg Cells In Lymphocytes Research Articles

Pathogenic mechanism of intestinal microbiota involved in Guillain-Barre syndrome and with Bifidobacterium intervention

IntroductionGuillain-barre syndrome (GBS) is an acute immune-mediated polyneuropathy, involving the peripheral nervous system. The pathogenicity of GBS lies on Th17/Treg imbalance which may be affected by intestinal microbiota. From the previous study, treatment with Bifidobacterium infantis (B. infantis) significantly improved the symptoms of experimental autoimmune neuritis (EAN) through reducing the levels of IL-17A. In the present study, we aimed to further investigate the pathogenic mechanisms of intestinal microbiota involved in GBS, with the intervention of Bifidobacterium.Material and methodsLewis rats (n = 18) were injected with P253-78 peptide and completed Freund's adjuvant to induce EAN model. The clinical scores, Hematoxylin–eosin (HE) staining and transmission electron microscopy at day 15 after immunization were used to determine the pathological changes. The levels of IL-17, IL-10 and TGF-β and the proportions of Th17 and Treg cells in lymphocytes of blood samples were used to decide the Th17 / Treg imbalance. The intestinal microbiota was detected using 16S rRNA technology, and the bacteria with significant changes were also detected in fecal specimens of GBS patients.ResultsB. infantis improved EAN, by decreasing clinical scores and pathological changes, thus improving Th17/Treg imbalance. Moreover, the number of Lactobacillus, Rumenococcus and Clostridium were significantly reduced whereas the number of Akkermansia, Escherichia and Coprococcus significantly increased in the EAN group, which was abrogated by B. infantis.ConclusionsImbalance of Th17/Tregs expression induced by imbalance of intestinal microbiota may get involved in GBS. However, B. infantis intervention can regulate Th17/Treg balance by regulating imbalanced intestinal microbiota, thus improving GBS.

Cucurbitacin IIb improved active chromatin-induced systemic lupus erythematosus via balancing the percentage of Th17 and Treg cells.

The pathogenesis of systemic lupus erythematosus (SLE) is closely associated with aberrant immune system. Here, the aim of our study was to explore the regulation of cucurbitacin IIb (CuIIb) to Th17/Treg cells in SLE. Compared with normal mice, the percentage of Treg cells was downregulated in SLE mouse model, and Th17 was upregulated. Meantime, the production of Treg-related transcription factor (foxp3) in SLE model mouse was reduced, and the production of Th17-related transcription factor (RORγt) was increased. After treatment with CuIIb, the percentage of Treg cells in SLE mice was partly upregulated, and Th17 cells percentage was downregulated. The expression of foxp3 and RORγt in SLE mice were promoted and inhibited by CuIIb treatment, respectively. SLE-induced kidney injury also was improved by CuIIb treatment. In vitro, we demonstrated again that CuIIb upregulated the percentage of Treg cells in lymphocytes from SLE mice, and downregulated the percentage of Th17 cells. Highly expressed IL-6 and IL17, and lowly expressed IL-10 and TGF-β in lymphocytes from SLE mice were repressed and facilitated by CuIIb treatment, respectively. Overall, our data proved that CuIIb improved kidney injury in SLE mice through balancing the percentage of Th17 and Treg cells. Our data provided a reliable evidence to support the potential of CuIIb in SLE treatment.