Intestinal barrier dysfunction following traumatic brain injury

2019 ◽  
Vol 40 (6) ◽  
pp. 1105-1110 ◽  
Author(s):  
Pengfei Pan ◽  
Yunlin Song ◽  
Xinxin Du ◽  
Linlin Bai ◽  
Xiaoli Hua ◽  
...  
eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Rebeccah J Katzenberger ◽  
Stanislava Chtarbanova ◽  
Stacey A Rimkus ◽  
Julie A Fischer ◽  
Gulpreet Kaur ◽  
...  

Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Unfavorable TBI outcomes result from primary mechanical injuries to the brain and ensuing secondary non-mechanical injuries that are not limited to the brain. Our genome-wide association study of Drosophila melanogaster revealed that the probability of death following TBI is associated with single nucleotide polymorphisms in genes involved in tissue barrier function and glucose homeostasis. We found that TBI causes intestinal and blood–brain barrier dysfunction and that intestinal barrier dysfunction is highly correlated with the probability of death. Furthermore, we found that ingestion of glucose after a primary injury increases the probability of death through a secondary injury mechanism that exacerbates intestinal barrier dysfunction. Our results indicate that natural variation in the probability of death following TBI is due in part to genetic differences that affect intestinal barrier dysfunction.


2015 ◽  
Author(s):  
Rebeccah J Katzenberger ◽  
Stanislava Chtarbanova ◽  
Stacey A Rimkus ◽  
Julie A Fischer ◽  
Gulpreet Kaur ◽  
...  

2006 ◽  
Vol 51 (9) ◽  
pp. 1549-1556 ◽  
Author(s):  
Desheng Song ◽  
Bin Shi ◽  
Hua Xue ◽  
Yousheng Li ◽  
Xiaodong Yang ◽  
...  

2006 ◽  
Vol 41 (8) ◽  
pp. 1386-1391 ◽  
Author(s):  
Ali Nayci ◽  
Sibel Atis ◽  
Gulden Ersoz ◽  
Ayse Polat ◽  
Derya Talas

Amino Acids ◽  
2021 ◽  
Author(s):  
Tatsuya Hasegawa ◽  
Ami Mizugaki ◽  
Yoshiko Inoue ◽  
Hiroyuki Kato ◽  
Hitoshi Murakami

AbstractIntestinal oxidative stress produces pro-inflammatory cytokines, which increase tight junction (TJ) permeability, leading to intestinal and systemic inflammation. Cystine (Cys2) is a substrate of glutathione (GSH) and inhibits inflammation, however, it is unclear whether Cys2 locally improves intestinal barrier dysfunction. Thus, we investigated the local effects of Cys2 on oxidative stress-induced TJ permeability and intestinal inflammatory responses. Caco-2 cells were cultured in a Cys2-supplemented medium for 24 h and then treated with H2O2 for 2 h. We assessed TJ permeability by measuring transepithelial electrical resistance and the paracellular flux of fluorescein isothiocyanate–dextran 4 kDa. We measured the concentration of Cys2 and GSH after Cys2 pretreatment. The mRNA expression of pro-inflammatory cytokines was assessed. In addition, the levels of TJ proteins were assessed by measuring the expression of TJ proteins in the whole cells and the ratio of TJ proteins in the detergent-insoluble fractions to soluble fractions (IS/S ratio). Cys2 treatment reduced H2O2-induced TJ permeability. Cys2 did not change the expression of TJ proteins in the whole cells, however, suppressed the IS/S ratio of claudin-4. Intercellular levels of Cys2 and GSH significantly increased in cells treated with Cys2. Cys2 treatment suppressed the mRNA expression of pro-inflammatory cytokines, and the mRNA levels were significantly correlated with TJ permeability. In conclusion, Cys2 treatment locally reduced oxidative stress-induced intestinal barrier dysfunction possively due to the mitigation of claudin-4 dislocalization. Furthermore, the effect of Cys2 on the improvement of intestinal barrier function is related to the local suppression of oxidative stress-induced pro-inflammatory responses.


Sign in / Sign up

Export Citation Format

Share Document