scholarly journals Oxidative Stress Impact on Barrier Function of Porcine Angular Aqueous Plexus Cell Monolayers

2013 ◽  
Vol 54 (7) ◽  
pp. 4827 ◽  
Author(s):  
Yuan Lei ◽  
William D. Stamer ◽  
Jihong Wu ◽  
Xinghuai Sun
Keyword(s):  
Oxidative Stress ◽  
Barrier Function ◽  
Cell Monolayers ◽  
Plexus Cell

scholarly journals Catechin and Procyanidin B2 Modulate the Expression of Tight Junction Proteins but Do Not Protect from Inflammation-Induced Changes in Permeability in Human Intestinal Cell Monolayers

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2271 ◽  
Author(s):  
Massimiliano G. Bianchi ◽  
Martina Chiu ◽  
Giuseppe Taurino ◽  
Furio Brighenti ◽  
Daniele Del Rio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Barrier Function ◽  
Cell Model ◽  
Intestinal Cell ◽  
Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Inflammatory Stress ◽  
Cell Monolayers ◽  
Dietary Polyphenols ◽  
Junctional Proteins

The possibility of counteracting inflammation-related barrier defects with dietary compounds such as (poly)phenols has raised much interest, but information is still scarce. We have investigated here if (+)-catechin (CAT) and procyanidin B2 (PB2), two main dietary polyphenols, protect the barrier function of intestinal cells undergoing inflammatory stress. The cell model adopted consisted of co-cultured Caco-2 and HT29-MTX cells, while inflammatory conditions were mimicked through the incubation of epithelial cells with the conditioned medium of activated macrophages (MCM). The epithelial barrier function was monitored through trans-epithelial electrical resistance (TEER), and ROS production was assessed with dichlorofluorescein, while the expression of tight-junctional proteins and signal transduction pathways were evaluated with Western blot. The results indicated that MCM produced significant oxidative stress, the activation of NF-κB and MAPK pathways, a decrease in occludin and ZO-1 expression, and an increase in claudin-7 (CL-7) expression, while TEER was markedly lowered. Neither CAT nor PB2 prevented oxidative stress, transduction pathways activation, ZO-1 suppression, or TEER decrease. However, PB2 prevented the decrease in occludin expression and both polyphenols produced a huge increase in CL-7 abundance. It is concluded that, under the conditions adopted, CAT and PB2 do not prevent inflammation-dependent impairment of the epithelial barrier function of intestinal cell monolayers. However, the two compounds modify the expression of tight-junctional proteins and, in particular, markedly increase the expression of CL-7. These insights add to a better understanding of the potential biological activity of these major dietary flavan-3-ols at intestinal level.

scholarly journals Mechanisms of lung endothelial barrier disruption induced by cigarette smoke: role of oxidative stress and ceramides

2011 ◽  
Vol 301 (6) ◽  
pp. L836-L846 ◽  
Author(s):  
Kelly S. Schweitzer ◽  
Hadi Hatoum ◽  
Mary Beth Brown ◽  
Mehak Gupta ◽  
Matthew J. Justice ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
P38 Mapk ◽  
Barrier Function ◽  
Rho Kinase ◽  
Endothelial Barrier ◽  
Kinase Activation ◽  
Cell Monolayers ◽  
Neutral Sphingomyelinase ◽  
Soluble Components

The epithelial and endothelial cells lining the alveolus form a barrier essential for the preservation of the lung respiratory function, which is, however, vulnerable to excessive oxidative, inflammatory, and apoptotic insults. Whereas profound breaches in this barrier function cause pulmonary edema, more subtle changes may contribute to inflammation. The mechanisms by which cigarette smoke (CS) exposure induce lung inflammation are not fully understood, but an early alteration in the epithelial barrier function has been documented. We sought to investigate the occurrence and mechanisms by which soluble components of mainstream CS disrupt the lung endothelial cell barrier function. Using cultured primary rat microvascular cell monolayers, we report that CS induces endothelial cell barrier disruption in a dose- and time-dependent manner of similar magnitude to that of the epithelial cell barrier. CS exposure triggered a mechanism of neutral sphingomyelinase-mediated ceramide upregulation and p38 MAPK and JNK activation that were oxidative stress dependent and that, along with Rho kinase activation, mediated the endothelial barrier dysfunction. The morphological changes in endothelial cell monolayers induced by CS included actin cytoskeletal rearrangement, junctional protein zonula occludens-1 loss, and intercellular gap formation, which were abolished by the glutathione modulator N-acetylcysteine and ameliorated by neutral sphingomyelinase inhibition. The direct application of ceramide recapitulated the effects of CS, by disrupting both endothelial and epithelial cells barrier, by a mechanism that was redox and apoptosis independent and required Rho kinase activation. Furthermore, ceramide induced dose-dependent alterations of alveolar microcirculatory barrier in vivo, measured by two-photon excitation microscopy in the intact rat. In conclusion, soluble components of CS have direct endothelial barrier-disruptive effects that could be ameliorated by glutathione modulators or by inhibitors of neutral sphingomyelinase, p38 MAPK, JNK, and Rho kinase. Amelioration of endothelial permeability may alleviate lung and systemic vascular dysfunction associated with smoking-related chronic obstructive lung diseases.

scholarly journals Bacillus cereus Induces Permeability of an In Vitro Blood-Retina Barrier

2008 ◽  
Vol 76 (4) ◽  
pp. 1358-1367 ◽  
Author(s):  
A. L. Moyer ◽  
R. T. Ramadan ◽  
J. Thurman ◽  
A. Burroughs ◽  
M. C. Callegan
Keyword(s):  
Quorum Sensing ◽  
Bacillus Cereus ◽  
Barrier Function ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Toxin Production ◽  
Global Regulator ◽  
Barrier Permeability ◽  
Cell Monolayers

ABSTRACT Most Bacillus cereus toxin production is controlled by the quorum-sensing-dependent, pleiotropic global regulator plcR, which contributes to the organism's virulence in the eye. The purpose of this study was to analyze the effects of B. cereus infection and plcR-regulated toxins on the barrier function of retinal pigment epithelium (RPE) cells, the primary cells of the blood-retina barrier. Human ARPE-19 cells were apically inoculated with wild-type or quorum-sensing-deficient B. cereus, and cytotoxicity was analyzed. plcR-regulated toxins were not required for B. cereus-induced RPE cytotoxicity, but these toxins did increase the rate of cell death, primarily by necrosis. B. cereus infection of polarized RPE cell monolayers resulted in increased barrier permeability, independent of plcR-regulated toxins. Loss of both occludin and ZO-1 expression occurred by 8 h postinfection, but alterations in tight junctions appeared to precede cytotoxicity. Of the several proinflammatory cytokines analyzed, only interleukin-6 was produced in response to B. cereus infection. These results demonstrate the deleterious effects of B. cereus infection on RPE barrier function and suggest that plcR-regulated toxins may not contribute significantly to RPE barrier permeability during infection.

scholarly journals Arctigenin fromFructus Arctii(Seed of Burdock) Reinforces Intestinal Barrier Function in Caco-2 Cell Monolayers

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Hee Soon Shin ◽  
Sun Young Jung ◽  
Su Yeon Back ◽  
Jeong-Ryong Do ◽  
Dong-Hwa Shon
Keyword(s):  
Barrier Function ◽  
Active Component ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Transepithelial Electrical Resistance ◽  
Intestinal Barrier Function ◽  
Intestinal Epithelial ◽  
Traditional Herbal Medicine ◽  
Cell Monolayers ◽  
Basolateral Side

Fructus Arctiiis used as a traditional herbal medicine to treat inflammatory diseases in oriental countries. This study aimed to investigate effect ofF. Arctiiextract on intestinal barrier function in human intestinal epithelial Caco-2 cells and to reveal the active component ofF. Arctii. We measured transepithelial electrical resistance (TEER) value (as an index of barrier function) and ovalbumin (OVA) permeation (as an index of permeability) to observe the changes of intestinal barrier function. The treatment ofF. Arctiiincreased TEER value and decreased OVA influx on Caco-2 cell monolayers. Furthermore, we found that arctigenin as an active component ofF. Arctiiincreased TEER value and reduced permeability of OVA from apical to the basolateral side but not arctiin. In the present study, we revealed thatF. Arctiicould enhance intestinal barrier function, and its active component was an arctigenin on the functionality. We expect that the arctigenin fromF. Arctiicould contribute to prevention of inflammatory, allergic, and infectious diseases by reinforcing intestinal barrier function.

Abstract 561: Dysregulation of miR-155 in Acute Oscillatory Shear Stress (OSS)-mediated Oxidative Stress, Inflammation and Endothelial Dysfunction

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Islam Mohamed ◽  
Sheena Thomas ◽  
Kimberly Rooney ◽  
Roy Sutliff ◽  
Nick Willett ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Shear Stress ◽  
Barrier Function ◽  
Oscillatory Shear ◽  
Blue Dye ◽  
Down Regulation ◽  
Inflammatory Stress ◽  
Cytoskeleton Organization ◽  
Oscillatory Shear Stress

Introduction: Shear stress forces play an integral role in dictating the endothelial cell (EC) response to changes in blood flow, pro-inflammatory response and hence development of atherosclerosis. Previously, our group has identified EC microRNA-155 (miR-155) as one of the key signature dysregulated miRNAs in areas of chronic low magnitude oscillatory shear stress (OSS) in vasculature and OSS models of in-vitro. Hypothesis: we hypothesized that acute induction of OSS mediates EC oxidative stress, inflammation and dysfunction, via dysregulation of EC miR-155. Methods: 12-week old C57B/6J mice were subjected to abdominal aortic coarctation (AAC), a unique model of acute induction of OSS, for 3 days and downstream segments of acute OSS were compared to upstream unidirectional shear stress (USS) segments of the thoracic aorta. Results: Acute OSS resulted in down regulation of EC miR-155 expression and inverse upregulation of EC RhoA and Myosin light chain kinase (MYLK), known targets of miR-155-mediated EC cytoskeleton organization, in OSS segments compared with USS. This was associated with impaired EC dependent relaxation, differential contractile response to phenylephrine, and loss of EC barrier function as evaluated by extravasation of Evans-blue dye assay. In parallel, En-face immunohistochemical staining also showed increased expression of EC nitric oxide synthase (eNOS) along with increased levels of reactive oxygen species (ROS) and nitrotyrosine (NY) formation in OSS segments compared with USS. Conclusions: Together, our studies shed light on the early changes in EC response to acute induction of OSS and resulting down-regulation of EC mir-155, including; oxidative/inflammatory stress, EC dysfunction, loss of barrier function and cytoskeletal changes. Despite the early upregulation of eNOS, it could also potentially synergize with the activation of the RhoA-MYLK pathway in EC oxidative (ROS/NY)/inflammatory stress and associated EC dysfunction. Further studies are in progress to dissect the interplay between these different pathways and their causal relationships as downstream targets of EC miR-155.

Enteropathogenic Escherichia coli adherence to intestinal epithelial monolayers diminishes barrier function

1995 ◽  
Vol 268 (2) ◽  
pp. G374-G379 ◽  
Author(s):  
J. Spitz ◽  
R. Yuhan ◽  
A. Koutsouris ◽  
C. Blatt ◽  
J. Alverdy ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Host Cell ◽  
Barrier Function ◽  
Cell Function ◽  
Cytoskeletal Proteins ◽  
Calcium Stores ◽  
Intestinal Epithelial ◽  
Enteropathogenic Escherichia Coli ◽  
Wild Type ◽  
Cell Monolayers

The mechanism by which enteropathogenic Escherichia coli (EPEC) causes diarrhea remains elusive. Several alterations within the host cell have been demonstrated to occur following EPEC attachment including increases in intracellular Ca2+ concentration and rearrangement and phosphorylation of several cytoskeletal proteins. The consequences of these intracellular perturbations on host cell function, however, have not been determined. The aim of this study was to examine the effect of EPEC adherence on intestinal epithelial barrier function. T84 cell monolayers were infected with either wild-type EPEC or a nonadherent isogenic derivative. Transepithelial electrical resistance, a measure of barrier function, decreased 33.5 +/- 6.4% after a 6-h incubation with the wild-type strain. Electron microscopy revealed ultrastructurally normal cells, and lactate dehydrogenase release assays failed to demonstrate cytotoxicity. Dual 22Na+ and [3H]mannitol flux studies localized the permeability defect to tight junctions. In addition, cumulative flux of the paracellular marker mannitol was four- to fivefold greater across monolayers infected with wild-type EPEC. Sequestration of intracellular calcium stores by dantrolene completely abrogated the resistance drop associated with EPEC attachment. These data demonstrate that adherence of EPEC to intestinal epithelial cell monolayers disrupts tight junction barrier function via a calcium-requiring event.

scholarly journals Assessment of Human Skin Gene Expression by Different Blends of Plant Extracts with Implications to Periorbital Skin Aging

2018 ◽  
Vol 19 (11) ◽  
pp. 3349 ◽  
Author(s):  
Jin Namkoong ◽  
Dale Kern ◽  
Helen Knaggs
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Human Skin ◽  
Barrier Function ◽  
Skin Barrier ◽  
Skin Aging ◽  
Skin Barrier Function ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
And Oxidative Stress

Since the skin is the major protective barrier of the body, it is affected by intrinsic and extrinsic factors. Environmental influences such as ultraviolet (UV) irradiation, pollution or dry/cold air are involved in the generation of radical oxygen species (ROS) and impact skin aging and dermal health. Assessment of human skin gene expression and other biomarkers including epigenetic factors are used to evaluate the biological/molecular activities of key compounds in cosmetic formulas. The objective of this study was to quantify human gene expression when epidermal full-thickness skin equivalents were exposed to: (a) a mixture of betaine, pentylene glycol, Saccharomyces cerevisiae and Rhodiola rosea root extract (BlendE) for antioxidant, skin barrier function and oxidative stress (with hydrogen peroxide challenge); and (b) a mixture of Narcissus tazetta bulb extract and Schisandra chinensis fruit extract (BlendIP) for various biomarkers and microRNA analysis. For BlendE, several antioxidants, protective oxidative stress biomarkers and many skin barrier function parameters were significantly increased. When BlendE was evaluated, the negative impact of the hydrogen peroxide was significantly reduced for the matrix metalloproteinases (MMP 3 and MMP 12), the skin aging and oxidative stress biomarkers, namely FBN2, ANXA1 and HGF. When BlendIP was tested for cell proliferation and dermal structural components to enhance the integrity of the skin around the eyes: 8 growth factors, 7 signaling, 7 structural/barrier function and 7 oxidative stress biomarkers were significantly increased. Finally, when BlendIP was tested via real-time RT-PCR for microRNA expression: miR-146a, miR-22, miR155, miR16 and miR21 were all significantly increased over control levels. Therefore, human skin gene expression studies are important tools to assess active ingredient compounds such as plant extract blends to advance dermal hypotheses toward validating cosmetic formulations with botanical molecules.

scholarly journals Effects of Dietary Taurine Supplementation to Gilts during Late Gestation and Lactation on Offspring Growth and Oxidative Stress

Animals ◽  
2019 ◽  
Vol 9 (5) ◽  
pp. 220 ◽  
Author(s):  
Mengmeng Xu ◽  
Long Che ◽  
Kaiguo Gao ◽  
Li Wang ◽  
Xuefen Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Growth Performance ◽  
Barrier Function ◽  
Average Daily Gain ◽  
Basal Diet ◽  
Intestinal Morphology ◽  
Late Gestation ◽  
Villus Height ◽  
And Oxidative Stress

Birth is one of the most important events of animal production agriculture, as newborns are abruptly forced to adapt to environmental and nutritional disruptions that can lead to oxidative damage and delay in growth. Taurine (Tau) is an important regulator of oxidative stress and possesses growth-enhancing properties. In the present study, we investigated the effects of dietary Tau supplementation in gilts during late gestation and lactation on the growth performance of piglets by assessing intestinal morphology and barrier function, and oxidative stress status. Sixteen gilts were randomly allocated to the Con (basal diet) and Tau (basal diet with 1% Tau) groups from 75 d of gestation to weaning. Maternal dietary Tau supplementation significantly increased weaning weight and average daily gain weight in piglets. Piglets in the Tau group had higher villus height and villus height-to-crypt depth ratio (VCR), ZO-1 protein expression, and secretory immunoglobulin A (sIgA) content in the jejunum. Meanwhile, Tau bebeficial affected the milk quality of gilts, as indicated by decreased malondialdehyde (MDA) concentration and increased total superoxide dismutase (T-SOD), total antioxidative capability (T-AOC), glutathione peroxidase (GPx), and catalase (CAT) activity. Furthermore, Tau supplementation increased T-SOD activity in plasma and SOD2 protein expression in the jejunum in the piglets. In conclusion, this study provides evidence that dietary Tau supplementation to gilts improves growth performance in piglets, owing to improved intestinal morphology and barrier function, as well as inhibition of oxidative stress.

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