452 Effects of Lactobacillus reuteri LR1 on tight junction proteins expression in Ipec-1 cells during enterotoxigenic Escherichia coli K88 infection and its underlying mechanisms

2017 ◽  
Vol 95 (suppl_4) ◽  
pp. 222-222 ◽  
Author(s):  
L. Wang ◽  
H. Yi ◽  
Z. Wang ◽  
Y. Qiu ◽  
X. Wen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Tight Junction ◽  
Lactobacillus Reuteri ◽  
Enterotoxigenic Escherichia Coli ◽  
Tight Junction Proteins ◽  
Underlying Mechanisms ◽  
Junction Proteins

scholarly journals Tricellular Tight Junction Protein Tricellulin Is Targeted by the Enteropathogenic Escherichia coli Effector EspG1, Leading to Epithelial Barrier Disruption

2016 ◽  
Vol 85 (1) ◽  
Author(s):  
Vijay Morampudi ◽  
Franziska A. Graef ◽  
Martin Stahl ◽  
Udit Dalwadi ◽  
Victoria S. Conlin ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Tight Junction ◽  
Significant Loss ◽  
Effector Proteins ◽  
Epithelial Barrier ◽  
Tight Junction Proteins ◽  
Barrier Dysfunction ◽  
Barrier Disruption ◽  
Junction Protein ◽  
Junction Proteins

ABSTRACT Enteropathogenic Escherichia coli (EPEC)-induced diarrhea is often associated with disruption of intestinal epithelial tight junctions. Although studies have shown alterations in the expression and localization of bicellular tight junction proteins during EPEC infections, little is known about whether tricellular tight junction proteins (tTJs) are affected. Using Caco-2 cell monolayers, we investigated if EPEC is capable of targeting the tTJ protein tricellulin. Our results demonstrated that at 4 h postinfection, EPEC induced a significant reduction in tricellulin levels, accompanied by a significant loss of transepithelial resistance (TEER) and a corresponding increase in paracellular permeability. Conversely, cells overexpressing tricellulin were highly resistant to EPEC-induced barrier disruption. Confocal microscopy revealed the distribution of tricellulin into the plasma membrane of infected epithelial cells and confirmed the localization of EPEC aggregates in close proximity to tTJs. Moreover, infections with EPEC strains lacking genes encoding specific type III secreted effector proteins demonstrated a crucial role for the effector EspG1 in modulating tricellulin expression. Complementation studies suggest that the EspG-induced depletion of tricellulin is microtubule dependent. Overall, our results show that EPEC-induced epithelial barrier dysfunction is mediated in part by EspG1-induced microtubule-dependent depletion of tricellulin.

scholarly journals Neonatal Hyperoxia Downregulates Claudin-4, Occludin, and ZO-1 Expression in Rat Kidney Accompanied by Impaired Proximal Tubular Development

2020 ◽  
Vol 2020 ◽  
pp. 1-18
Author(s):  
Xuewen Xu ◽  
Xinyue Zhang ◽  
Linlin Gao ◽  
Chunfeng Liu ◽  
Kai You
Keyword(s):  
Tight Junction ◽  
Renal Injury ◽  
Rat Kidney ◽  
Proximal Tubules ◽  
Inflammatory Factors ◽  
Tight Junction Proteins ◽  
Tnf Α ◽  
Underlying Mechanisms ◽  
Neonatal Hyperoxia ◽  
Junction Proteins

Hyperoxia is essential to manage in preterm infants but causes injury to immature kidney. Previous study indicates that hyperoxia causes oxidative damage to neonatal kidney and impairs renal development. However, the underlying mechanisms by which neonatal hyperoxia effects on immature kidney still need to be elucidated. Tight junction, among which the representative proteins are claudin-4, occludin, and ZO-1, plays a crucial role in nephrogenesis and maintaining renal function. Inflammatory cytokines are involved in the pleiotropic regulation of tight junction proteins. Here, we investigated how neonatal hyperoxia affected the expression of key tight junction proteins and inflammatory factors (IL-6 and TNF-α) in the developing rat kidneys and elucidated their correlation with renal injury. We found claudin-4, occludin, and zonula occludens-1 (ZO-1) expression in proximal tubules was significantly downregulated after neonatal hyperoxia. The expression of these tight junction proteins was positively correlated with that of IL-6 and TNF-α, while claudin-4 expression was positively correlated with injury score of proximal tubules in mature kidneys. These findings indicated that impaired expression of tight junction proteins in kidney might be a potential mechanism of hyperoxia-induced nephrogenic disorders. It provides new insights to further study oxidative renal injury and development disorders and will be helpful for seeking potential therapeutics for hyperoxia-induced renal injury in the future.

scholarly journals Lactobacillus casei Zhang Counteracts Blood-Milk Barrier Disruption and Moderates the Inflammatory Response in Escherichia coli-Induced Mastitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yuhui Zheng ◽  
Gang Liu ◽  
Wei Wang ◽  
Yajing Wang ◽  
Zhijun Cao ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Inflammatory Response ◽  
Tight Junction ◽  
Lactobacillus Casei ◽  
Mammary Tissue ◽  
Tight Junction Proteins ◽  
E Coli ◽  
Tnf Α ◽  
Injury Models ◽  
Junction Proteins

Escherichia coli is a common mastitis-causing pathogen that can disrupt the blood-milk barrier of mammals. Although Lactobacillus casei Zhang (LCZ) can alleviate mice mastitis, whether it has a prophylactic effect on E. coli-induced mastitis through intramammary infusion, as well as its underlying mechanism, remains unclear. In this study, E. coli-induced injury models of bovine mammary epithelial cells (BMECs) and mice in lactation were used to fill this research gap. In vitro tests of BMECs revealed that LCZ significantly inhibited the E. coli adhesion (p < 0.01); reduced the cell desmosome damage; increased the expression of the tight junction proteins claudin-1, claudin-4, occludin, and zonula occludens-1 (ZO-1; p < 0.01); and decreased the expression of the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 (p < 0.01), thereby increasing trans-epithelial electric resistance (p < 0.01) and attenuating the lactate dehydrogenase release induced by E. coli (p < 0.01). In vivo tests indicated that LCZ significantly reduced the injury and histological score of mice mammary tissues in E. coli-induced mastitis (p < 0.01) by significantly promoting the expression of the tight junction proteins claudin-3, occludin, and ZO-1 (p < 0.01), which ameliorated blood-milk barrier disruption, and decreasing the expression of the inflammatory cytokines (TNF-α, IL-1β, and IL-6) in mice mammary tissue (p < 0.01). Our study suggested that LCZ counteracted the disrupted blood-milk barrier and moderated the inflammatory response in E. coli-induced injury models, indicating that LCZ can ameliorate the injury of mammary tissue in mastitis.

scholarly journals Lactobacillus reuteri LR1 Improved Expression of Genes of Tight Junction Proteins via the MLCK Pathway in IPEC-1 Cells during Infection with Enterotoxigenic Escherichia coli K88

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Hongbo Yi ◽  
Li Wang ◽  
Yunxia Xiong ◽  
Zhilin Wang ◽  
Yueqin Qiu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Tight Junction ◽  
Lactobacillus Reuteri ◽  
Transcript Abundance ◽  
Enterotoxigenic Escherichia Coli ◽  
Epithelial Barrier ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function

Intestinal epithelial barrier damage disrupts immune homeostasis and leads to many intestinal disorders. Lactobacillus reuteri strains have probiotic functions in their modulation of the microbiota and immune system in intestines. In this study, the effects of L. reuteri LR1, a new strain isolated from the feces of weaning piglets, on intestinal epithelial barrier damage in IPEC-1 cells caused by challenge with enterotoxigenic Escherichia coli (ETEC) K88 were examined. It was found that L. reuteri LR1, in large part, offset the ETEC K88-induced increase in permeability of IPEC-1 cell monolayers and decreased the adhesion and invasion of the coliform in IPEC-1 cells. In addition, L. reuteri LR1 increased transcript abundance and protein contents of tight junction (TJ) proteins zonula occluden-1 (ZO-1) and occludin in ETEC K88-infected IPEC-1 cells, whereas it had no effects on claudin-1 and F-actin expression. Using colloidal gold immunoelectron microscopy, these effects of L. reuteri LR1 on ZO-1 and occludin content in IPEC-1 cells were confirmed. By using ML-7, a selective inhibitor of myosin light-chain kinase (MLCK), the beneficial effect of L. reuteri LR1 on contents of ZO-1 and occludin was shown to be dependent on the MLCK pathway. In conclusion, L. reuteri LR1 had beneficial effects on epithelial barrier function consistent with increasing ZO-1 and occludin expression via a MLCK-dependent manner in IPEC-1 cells during challenge with ETEC K88.

scholarly journals Modulation of Tight Junction Proteins in the Perineurium to Facilitate Peripheral Opioid Analgesia

2012 ◽  
Vol 116 (6) ◽  
pp. 1323-1334 ◽  
Author(s):  
Heike L. Rittner ◽  
Salah Amasheh ◽  
Rabih Moshourab ◽  
Dagmar Hackel ◽  
Reine-Solange Yamdeu ◽  
...  
Keyword(s):  
Tight Junction ◽  
Tight Junction Proteins ◽  
Hydrophilic Drugs ◽  
Electrophysiological Recordings ◽  
Male Wistar Rats ◽  
Peripheral Opioid Analgesia ◽  
Underlying Mechanisms ◽  
Peripheral Opioid Receptors ◽  
Junction Proteins

Background Peripheral application of opioids reduces inflammatory pain but is less effective in noninflamed tissue of rats and human patients. Hypertonic solutions can facilitate the antinociceptive activity of hydrophilic opioids in noninflamed tissue in vivo. However, the underlying mechanisms are not well understood. We hypothesized that the enhanced efficacy of opioids may be because of opening of the perineurial barrier formed by tight junction-proteins like claudin-1. Methods Male Wistar rats were treated intraplantarly with 10% NaCl. Pain behavior (n = 6) and electrophysiological recordings (n = 9 or more) from skin-nerve preparations after local application of the opioid [d-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAMGO) were explored. Tight junction-proteins as well as permeability of the barrier were examined by immunohistochemistry and Western blot (n = 3 or more). Results Local administration of 10% NaCl facilitated increased mechanical nociceptive thresholds in response to DAMGO, penetration of horseradish peroxidase into the nerve, as well as a reduced response of C- but not Aδ-nociceptors to mechanical stimulation after application of DAMGO in the skin-nerve preparation. In noninflamed paw tissue, claudin-1 was expressed in the epidermis, blood vessels, and the perineurium, surrounding neurons immunoreactive for calcitonin gene-related peptide or protein gene product 9.5. Claudin-1 but not claudin-5 or occludin was significantly reduced after pretreatment with 10% NaCl. Intraplantar application of a metalloproteinase inhibitor (GM6001) completely reversed these effects. Conclusion Hypertonic saline opens the perineurial barrier via metalloproteinase activation and claudin-1 regulation, thereby allowing access of hydrophilic drugs to peripheral opioid receptors. This principle may be used to specifically target hydrophilic drugs to peripheral neurons.

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