Perturbation of gut microbiota plays an important role in micro/nanoplastics-induced gut barrier dysfunction

Nanoscale ◽  
2021 ◽  
Author(s):  
Jiyan Qiao ◽  
Rui Chen ◽  
Mengjie Wang ◽  
Ru Bai ◽  
Xuejing Cui ◽  
...  

Exposure to micro/nanoplastics (M/NPLs) deteriorates the intestinal barrier by disturbing the bacterial composition in the gut.

2019 ◽  
Vol 10 (10) ◽  
pp. 6517-6532 ◽  
Author(s):  
Hang Xu ◽  
Chunfang Zhao ◽  
Yutian Li ◽  
Ruiyu Liu ◽  
Mingzhang Ao ◽  
...  

Pyracantha fortuneana fruit extract (PFE) exhibits beneficial effects on IBF in association with the modulation of glycolipid digestion and gut microbiota in HFD-fed obese rats.


2020 ◽  
Vol 11 ◽  
Author(s):  
Qiulan Lv ◽  
Daxing Xu ◽  
Xuezhi Zhang ◽  
Xiaomin Yang ◽  
Peng Zhao ◽  
...  

BackgroundMore than 30–40% of uric acid is excreted via the intestine, and the dysfunction of intestinal epithelium disrupts uric acid excretion. The involvement of gut microbiota in hyperuricemia has been reported in previous studies, but the changes and mechanisms of intestinal immunity in hyperuricemia are still unknown.MethodsThis study developed a urate oxidase (Uox)-knockout (Uox–/–) mouse model for hyperuricemia using CRISPR/Cas9 technology. The lipometabolism was assessed by measuring changes in biochemical indicators. Furthermore, 4-kDa fluorescein isothiocyanate–labeled dextran was used to assess gut barrier function. Also, 16S rRNA sequencing was performed to examine the changes in gut microbiota in mouse feces. RNA sequencing, Western blot, Q-PCR, ELISA, and immunohistochemical analysis were used for measuring gene transcription, the number of immune cells, and the levels of cytokines in intestinal tissues, serum, kidney, liver, pancreas, and vascellum.ResultsThis study showed that the abundance of inflammation-related microbiota increased in hyperuricemic mice. The microbial pattern recognition–associated Toll-like receptor pathway and inflammation-associated TNF and NF-kappa B signaling pathways were significantly enriched. The increased abundance of inflammation-related microbiota resulted in immune disorders and intestinal barrier dysfunction by upregulating TLR2/4/5 and promoting the release of IL-1β and TNF-α. The levels of epithelial tight junction proteins occludin and claudin-1 decreased. The expression of the pro-apoptotic gene Bax increased. The levels of LPS and TNF-α in systemic circulation increased in hyperuricemic mice. A positive correlation was observed between the increase in intestinal permeability and serum levels of uric acid.ConclusionHyperuricemia was characterized by dysregulated intestinal immunity, compromised intestinal barrier, and systemic inflammation. These findings might serve as a basis for future novel therapeutic interventions for hyperuricemia.


2020 ◽  
Vol 11 (9) ◽  
pp. 8077-8088
Author(s):  
Zhenxia Xu ◽  
Wenchao Chen ◽  
Qianchun Deng ◽  
Qingde Huang ◽  
Xu Wang ◽  
...  

Intestinal epithelial barrier dysfunction with dysbiosis of gut microbiota contributes to the occurrence and acceleration of colitis.


2021 ◽  
Author(s):  
Jianzhao Liao ◽  
Quanwei Li ◽  
Chaiqin Lei ◽  
Wenlan Yu ◽  
Jichang Deng ◽  
...  

Copper (Cu) is an essential trace mineral, but the excessive intake can lead to potentially toxic effects on host physiology. The mammalian intestine harbors various microorganisms, which are associated with intestinal...


2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Zhongqi Li ◽  
Jian Li ◽  
Shouwei Zhang ◽  
Gang Chen ◽  
Shaohua Chi ◽  
...  

Abstract Intestinal barrier dysfunction has been implicated in the development of multiorgan dysfunction syndrome caused by the trauma-hemorrhagic shock (THS). However, the mechanisms underlying THS-induced gut barrier injury are still poorly understood. In the present study, we used the metabolomics analysis to test the hypothesis that altered metabolites might be related to the development of THS-induced barrier dysfunction in the large intestine. Under the induction of THS, gut barrier failure was characterized by injury of permeability and mucus layer, which were companied by the decreased expression of zonula occludens-1 in the colon and increased levels of inflammatory factors including tumor necrosis factor-α, interferon-γ, interleukin (IL)-6, and IL-1β in the serum. A total of 16 differential metabolites were identified in colonic tissues from THS-treated rats compared with control rats. These altered metabolites included dihydroxy acetone phosphate, ribose-5-phosphate, fructose, glyceric acid, succinic acid, and adenosine, which are critical intermediates or end products that are involved in pentose phosphate pathway, glycolysis, and tricarboxylic acid cycle as well as mitochondrial adenosine triphosphate biosynthesis. These findings may offer important insight into the metabolic alterations in THS-treated gut injury, which will be helpful for developing effective metabolites-based strategies to prevent THS-induced gut barrier dysfunction.


Author(s):  
Natalia Di Tommaso ◽  
Antonio Gasbarrini ◽  
Francesca Romana Ponziani

The intestinal mucosa provides a selective permeable barrier for nutrient absorption and protection from external factors. It consists of epithelial cells, immune cells and their secretions. The gut microbiota participates in regulating the integrity and function of the intestinal barrier in a homeostatic balance. Pathogens, xenobiotics and food can disrupt the intestinal barrier, promoting systemic inflammation and tissue damage. Genetic and immune factors predispose individuals to gut barrier dysfunction, and changes in the composition and function of the gut microbiota are central to this process. The progressive identification of these changes has led to the development of the concept of ‘leaky gut syndrome’ and ‘gut dysbiosis’, which underlie the relationship between intestinal barrier impairment, metabolic diseases and autoimmunity. Understanding the mechanisms underlying this process is an intriguing subject of research for the diagnosis and treatment of various intestinal and extraintestinal diseases.


2021 ◽  
Author(s):  
Chengcheng Yang ◽  
Yao Du ◽  
Daoyuan Ren ◽  
Xingbin Yang ◽  
Yan Zhao

Gut barrier dysfunction is triggered by gut microbiota dysbiosis that is closely associated with ulcerative colitis. Here, we first studied the prophylactic capacity of turmeric polysaccharides (TPS) to ameliorate dextran...


Sign in / Sign up

Export Citation Format

Share Document