scholarly journals Asymptomatic Hyperamylasemia in Stevens-Johnson Syndrome Is Associated with Intestinal Barrier Dysfunction

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Yujen Tseng ◽  
Zhongguang Luo ◽  
Hongyang Zhang ◽  
Chengfeng Zhang ◽  
Jian Chen
Keyword(s):  
Serum Amylase ◽  
Intestinal Barrier ◽  
Stevens Johnson Syndrome ◽  
Fecal Occult Blood ◽  
Study Cohort ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Johnson Syndrome ◽  
Junction Protein ◽  
Clinical Awareness

Background/Objectives. Stevens-Johnson syndrome (SJS) is an allergic disease characterized by extensive epidermal detachment and mucositis. SJS involves both the skin and mucosal membranes, including the gastrointestinal tract. The present study is aimed at understanding the underlying reason of asymptomatic hyperamylasemia in patients with SJS, which may be associated with mucosal injury of the GI tract. Methods. A retrospective study on SJS patients was conducted at a tertiary medical center. All patients diagnosed as SJS, with available serum amylase index, were included. Clinical data of all subjects were retrospectively collected and analyzed. Colonic mucosal biopsies were obtained to measure tight junction protein expression. Results. A total of nine patients were included in the present study for study analysis. The average serum amylase of the study cohort was 228.78 ± 204.18   U / L . Among which, five patients had a positive fecal occult blood test (FOBT). Colonic mucosal biopsies were obtained and stained with occludin and zonula occludens-1 (ZO-1). The expression of occludin and ZO-1 was significantly downregulated in SJS patients ( p < 0.01 ), which was indicative of intestinal barrier dysfunction. Conclusion. Hyperamylasemia often extends beyond pancreatic diseases. Clinical awareness of asymptomatic hyperamylasemia secondary to other systemic diseases can help avoid unnecessary overexamination and overtreatment.

scholarly journals A novel membrane protein Hoka regulates septate junction organization and stem cell homeostasis in the Drosophila gut

2020 ◽  
Author(s):  
Yasushi Izumi ◽  
Kyoko Furuse ◽  
Mikio Furuse
Keyword(s):  
Stem Cell ◽  
Membrane Protein ◽  
Intestinal Barrier ◽  
Septate Junction ◽  
Barrier Dysfunction ◽  
Septate Junctions ◽  
Cell Homeostasis ◽  
Intestinal Barrier Dysfunction ◽  
Epithelial Tumors ◽  
Junction Protein

AbstractSmooth septate junctions (sSJs) regulate the paracellular transport in the intestinal and renal system in arthropods. In Drosophila, the organization and physiological function of sSJs are regulated by at least three sSJ-specific membrane proteins: Ssk, Mesh, and Tsp2A. Here, we report a novel sSJ membrane protein Hoka, which has a single membrane-spanning segment with a short extracellular region having 13-amino acids, and a cytoplasmic region with three repeats of the Tyr-Thr-Pro-Ala motif. The larval midgut in hoka-mutants shows a defect in sSJ structure. Hoka forms a complex with Ssk, Mesh, and Tsp2A and is required for the correct localization of these proteins to sSJs. Knockdown of hoka in the adult midgut leads to intestinal barrier dysfunction, stem cell overproliferation, and epithelial tumors. In hoka-knockdown midguts, aPKC is up-regulated in the cytoplasm and the apical membrane of epithelial cells. The depletion of aPKC and yki in hoka-knockdown midguts results in reduced stem cell overproliferation. These findings indicate that Hoka cooperates with the sSJ-proteins Ssk, Mesh, and Tsp2A to organize sSJs, and is required for maintaining intestinal stem cell homeostasis through the regulation of aPKC and Yki activities in the Drosophila midgut.Summary statementDepletion of hoka, a gene encoding a novel septate junction protein, from the Drosophila midgut results in the disruption of septate junctions, intestinal barrier dysfunction, stem cell overproliferation, and epithelial tumors.

scholarly journals Intestinal Barrier Dysfunction Exacerbates Neuroinflammation via the TLR4 Pathway in Mice With Heart Failure

2021 ◽  
Vol 12 ◽  
Author(s):  
Jun-Yu Huo ◽  
Wan-Ying Jiang ◽  
Ting Yin ◽  
Hai Xu ◽  
Yi-Ting Lyu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Intestinal Permeability ◽  
Intestinal Barrier ◽  
Sham Operation ◽  
Barrier Dysfunction ◽  
Intestinal Alkaline Phosphatase ◽  
Intestinal Barrier Dysfunction ◽  
Junction Protein ◽  
Elevated Expression ◽  
The Brain

AimsThe present study aimed to investigate alterations in neuroinflammation after heart failure (HF) and explore the potential mechanisms.MethodsMale wild-type (WT) and Toll-like receptor 4 (TLR4)-knockout (KO) mice were subjected to sham operation or ligation of the left anterior descending coronary artery to induce HF. 8 weeks later, cardiac functions were analyzed by echocardiography, and intestinal barrier functions were examined by measuring tight junction protein expression, intestinal permeability and plasma metabolite levels. Alterations in neuroinflammation in the brain were examined by measuring microglial activation, inflammatory cytokine levels and the proinflammatory signaling pathway. The intestinal barrier protector intestinal alkaline phosphatase (IAP) and intestinal homeostasis inhibitor L-phenylalanine (L-Phe) were used to examine the relationship between intestinal barrier dysfunction and neuroinflammation in mice with HF.ResultsEight weeks later, WT mice with HF displayed obvious increases in intestinal permeability and plasma lipopolysaccharide (LPS) levels, which were accompanied by elevated expression of TLR4 in the brain and enhanced neuroinflammation. Treatment with the intestinal barrier protector IAP significantly attenuated neuroinflammation after HF while effectively increasing plasma LPS levels. TLR4-KO mice showed significant improvements in HF-induced neuroinflammation, which was not markedly affected by intestinal barrier inhibitors or protectors.ConclusionHF could induce intestinal barrier dysfunction and increase gut-to-blood translocation of LPS, which could further promote neuroinflammation through the TLR4 pathway.

Confirmation and Prevention of Intestinal Barrier Dysfunction and Bacterial Translocation Caused by Methotrexate

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

Oxygen supplementation during airway instrumentation improves intestinal barrier dysfunction

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

scholarly journals Cystine reduces tight junction permeability and intestinal inflammation induced by oxidative stress in Caco-2 cells

Amino Acids ◽  
2021 ◽  
Author(s):  
Tatsuya Hasegawa ◽  
Ami Mizugaki ◽  
Yoshiko Inoue ◽  
Hiroyuki Kato ◽  
Hitoshi Murakami
Keyword(s):  
Oxidative Stress ◽  
Tight Junction ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Whole Cells ◽  
Intestinal Barrier Dysfunction ◽  
Pro Inflammatory Cytokines

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.

Procyanidin A1 and its digestive products prevent acrylamide-induced intestinal barrier dysfunction via the MAPK-mediated MLCK pathway

2021 ◽  
Author(s):  
Fangfang Yan ◽  
Wanbing Chen ◽  
Li Zhao ◽  
Qun Lu ◽  
Chengming Wang ◽  
...  
Keyword(s):  
Small Intestine ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Gastrointestinal Digestion ◽  
Intestinal Barrier Dysfunction

Procyanidins can alleviate small intestine damage induced by acrylamide (ACR). However, little is known about whether procyanidins after gastrointestinal digestion can prevent ACR-induced intestinal barrier damage and the possible mechanism....

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