scholarly journals The gut microbiota engages different signaling pathways to induce Duox2 expression in the ileum and colon epithelium

2014 ◽  
Vol 8 (2) ◽  
pp. 372-379 ◽  
Author(s):  
F Sommer ◽  
F Bäckhed
2021 ◽  
Vol 69 (35) ◽  
pp. 10151-10162
Author(s):  
Ming-Yu Jin ◽  
Xiao-Yong Wu ◽  
Mei-Ying Li ◽  
Xiao-Tong Li ◽  
Ri-Ming Huang ◽  
...  

RSC Advances ◽  
2019 ◽  
Vol 9 (65) ◽  
pp. 37947-37956
Author(s):  
Wen Xiong ◽  
Haoyue Ma ◽  
Zhu Zhang ◽  
Meilan Jin ◽  
Jian Wang ◽  
...  

This study investigated the effects of icariin on intestinal barrier function and its underlying mechanisms.


2020 ◽  
Vol 78 (Supplement_1) ◽  
pp. 21-28
Author(s):  
Shengmin Sang ◽  
Emmanuel Idehen ◽  
Yantao Zhao ◽  
YiFang Chu

Abstract Although the biological mechanisms surrounding the widely reported association between whole grain (WG) consumption and reduced risk of several diseases are not fully understood, there is growing evidence suggesting that inflammation may be an essential mediator in this multifaceted process. It also appears that several mechanisms influence the modulatory actions of WGs on inflammation, including the effect of fiber, phytochemicals, and their microbial-derived metabolites. While some of these effects are direct, others involve gut microbiota, which transform important bioactive substances into more useful metabolites that moderate inflammatory signaling pathways. This review evaluates emerging evidence of the relationship between WGs and their effects on markers of subclinical inflammation, and highlights the role of fiber, unique WG phytochemicals, and gut microbiota on the anti-inflammatory effects of WG intake.


Apmis ◽  
2022 ◽  
Author(s):  
Astrid L.B. Bennedsen ◽  
Sara Furbo ◽  
Thomas Bjarnsholt ◽  
Hans Raskov ◽  
Ismail Gögenur ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Wei-jie Lv ◽  
Cui Liu ◽  
Lin-zeng Yu ◽  
Jia-hao Zhou ◽  
Yue Li ◽  
...  

There is a bidirectional relationship between inflammatory bowel disease (IBD) and depression/anxiety. Emerging evidences indicate that the liver may be involved in microbiota-gut-brain axis. This experiment focused on the role of melatonin in regulating the gut microbiota and explores its mechanism on dextran sulphate sodium- (DSS-) induced neuroinflammation and liver injury. Long-term DSS-treatment increased lipopolysaccharide (LPS), proinflammation cytokines IL-1β and TNF-α, and gut leak in rats, breaking blood-brain barrier and overactivated astrocytes and microglia. Ultimately, the rats showed depression-like behavior, including reduction of sucrose preference and central time in open field test and elevation of immobility time in a forced swimming test. Oral administration with melatonin alleviated neuroinflammation and depression-like behaviors. However, melatonin supplementation did not decrease the level of LPS but increase short-chain fatty acid (SCFA) production to protect DSS-induced neuroinflammation. Additionally, western blotting analysis suggested that signaling pathways farnesoid X receptor-fibroblast growth factor 15 (FXR-FGF 15) in gut and apoptosis signal-regulating kinase 1 (ASK1) in the liver overactivated in DSS-treated rats, indicating liver metabolic disorder. Supplementation with melatonin markedly inhibited the activation of these two signaling pathways and its downstream p38. As for the gut microbiota, we found that immune response- and SCFA production-related microbiota, like Lactobacillus and Clostridium significantly increased, while bile salt hydrolase activity-related microbiota, like Streptococcus and Enterococcus, significantly decreased after melatonin supplementation. These altered microbiota were consistent with the alleviation of neuroinflammation and metabolic disorder. Taken together, our findings suggest melatonin contributes to reshape gut microbiota and improves inflammatory processes in the hippocampus (HPC) and metabolic disorders in the liver of DSS rats.


2022 ◽  
Vol 12 ◽  
Author(s):  
Sajid Ur Rahman ◽  
Haiyan Gong ◽  
Rongsheng Mi ◽  
Yan Huang ◽  
Xiangan Han ◽  
...  

Cryptosporidium parvum infection is very common in infants, immunocompromised patients, or in young ruminants, and chitosan supplementation exhibits beneficial effects against the infection caused by C. parvum. This study investigated whether chitosan supplementation modulates the gut microbiota and mediates the TLR4/STAT1 signaling pathways and related cytokines to attenuate C. parvum infection in immunosuppressed mice. Immunosuppressed C57BL/6 mice were divided into five treatment groups. The unchallenged mice received a basal diet (control), and three groups of mice challenged with 1 × 106 C. parvum received a basal diet, a diet supplemented with 50 mg/kg/day paromomycin, and 1 mg/kg/day chitosan, and unchallenged mice treated with 1 mg/kg/day chitosan. Chitosan supplementation regulated serum biochemical indices and significantly (p < 0.01) reduced C. parvum oocyst excretion in infected mice treated with chitosan compared with the infected mice that received no treatment. Chitosan-fed infected mice showed significantly (p < 0.01) decreased mRNA expression levels of interferon-gamma (IFN-γ) and tumor necrosis factor-α (TNF-α) compared to infected mice that received no treatment. Chitosan significantly inhibited TLR4 and upregulated STAT1 protein expression (p < 0.01) in C. parvum-infected mice. 16S rRNA sequencing analysis revealed that chitosan supplementation increased the relative abundance of Bacteroidetes/Bacteroides, while that of Proteobacteria, Tenericutes, Defferribacteres, and Firmicutes decreased (p < 0.05). Overall, the findings revealed that chitosan supplementation can ameliorate C. parvum infection by remodeling the composition of the gut microbiota of mice, leading to mediated STAT1/TLR4 up- and downregulation and decreased production of IFN-γ and TNF-α, and these changes resulted in better resolution and control of C. parvum infection.


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