scholarly journals Effect of High Sulfur Diet on Rumen Fermentation, Microflora, and Epithelial Barrier Function in Steers

Animals ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 2545
Author(s):  
Hao Wu ◽  
Yan Li ◽  
Qingxiang Meng ◽  
Zhenming Zhou
Keyword(s):  
Hydrogen Sulfide ◽  
Barrier Function ◽  
Rumen Fermentation ◽  
Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Rumen Epithelium ◽  
Junction Protein ◽  
Production Of Hydrogen ◽  
Animal Feeding

These experiments were conducted to evaluate the effect of excessive sulfur on rumen fermentation, microflora, and epithelial barrier function in steers through in vitro gas production and animal feeding experiments. Nine and four levels of sulfur addition were evaluated in in vitro ruminal fermentation and animal feeding experiment, respectively. The results showed that increasing the level of sulfur in substrates decreased the total gas and methane production linearly, while increasing the production of hydrogen sulfide gas (p < 0.01). Volatile fatty acid concentrations, especially that of butyric acid, were increased by extra sulfur (p < 0.01). Sulfur content in the diet had no significant effect (p > 0.05) on most of the rumen microbes, except for Desulfovibrio, one of the major sulfate-reducing bacteria (SRB) in the rumen, whose population increased by adding extra sulfur (p < 0.001). The changes in the morphology of rumen epithelium and thickening of the total epithelial layer were mainly attributed to the increase in the acanthosis cell layer and stratum basale (p < 0.05). Further, the relative expressions of two tight junction protein regulating genes, CLDN-1 and TJP1, were reduced (p < 0.05). Excessive sulfur in the diet can change the type of rumen fermentation, sulfate metabolism and SRB population, and the rumen epithelial barrier function. The results of this study demonstrated that sulfur can be used as a methane inhibitor with the mechanism that SRB competitively used protons to produce hydrogen sulfide. However, a higher level of sulfur in the diet could increase the inflammatory reaction of the rumen epithelium which may affect nutrient absorption.

scholarly journals Effect of High Sulfur Diet on Rumen Fermentation, Microflora and Epithelial Barrier Function in Steers

2020 ◽  
Author(s):  
Hao Wu ◽  
Yan Li ◽  
Qingxiang Meng ◽  
Zhenming Zhou
Keyword(s):  
Barrier Function ◽  
Animal Health ◽  
Underlying Mechanism ◽  
Rumen Fermentation ◽  
Gas Production ◽  
Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Volatile Fatty Acid Concentration ◽  
Junction Protein

Abstract Background: Sulfur is essential for maintaining animal health and functional processing, but high sulfur in the diet can be toxic. The underlying mechanism for this toxicity is not clear in ruminants. Thus, we conducted experiments to evaluate the effect of excessive sulfur on rumen fermentation, microflora, and epithelial barrier function in steers through in vitro gas production and animal feeding trials.Results: The results showed that increasing the level of sulfur in substrates, decreased the total gas and methane production linearly while increasing the hydrogen sulfide gas (P<0.01). Though the high sulfur diet did not affect the rumen fermentation parameters (P>0.05), the volatile fatty acid concentration, especially the butyric acid, was increased by extra sulfur (P<0.01). Sulfur content in the diet had no significant effect (P>0.05) on most of the rumen microbes, expect Desulfovibrio, one of the major sulfate-reducing bacteria (SRB) in the rumen, whose population increased by adding extra sulfur (P<0.001). Changes in the morphology of rumen epithelium and thickening of the total epithelial layer were mainly attributed to the increase in the acanthosis cell layer and stratum basale (P<0.05). Also, the relative expression of two tight junction protein regulating genes, CLDN-1 and TJP1, were reduced with an increase in sulfur level in the diet (P<0.05).Conclusion: These results indicate that excessive sulfur in the diet can change the type of rumen fermentation, sulfate metabolism and SRB population, and the rumen epithelial barrier function.

scholarly journals Laminin-driven Epac/Rap1 regulation of epithelial barriers on decellularized matrix

2019 ◽  
Author(s):  
Bethany M. Young ◽  
Keerthana Shankar ◽  
Cindy K. Tho ◽  
Amanda R. Pellegrino ◽  
Rebecca L. Heise
Keyword(s):  
Barrier Function ◽  
Cellular Response ◽  
Alveolar Epithelium ◽  
Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Main Challenge ◽  
Barrier Formation ◽  
Epithelial Barriers ◽  
Molecular Therapeutic

ABSTRACTDecellularized tissues offer a unique tool for developing regenerative biomaterials orin vitroplatforms for the study of cell-extracellular matrix (ECM) interactions. One main challenge associated with decellularized lung tissue is that ECM components can be stripped away or altered by the detergents used to remove cellular debris. Without characterizing the composition of lung decellularized ECM (dECM) and the cellular response caused by the altered composition, it is difficult to utilize dECM for regeneration and specifically, engineering the complexities of the alveolar-capillary barrier. This study takes steps towards uncovering if dECM must be enhanced with lost ECM proteins to achieve proper epithelial barrier formation. To achieve this, epithelial barrier function was assessed on dECM coatings with and without the systematic addition of several key basement membrane proteins. After comparing barrier function on collagen, fibronectin, laminin, and dECM in varying combinations as anin vitrocoating, the alveolar epithelium exhibited superior barrier function when dECM was supplemented with laminin as evidenced by trans-epithelial electrical resistance (TEER) and permeability assays. Increased barrier resistance with laminin addition was associated with upregulation of Claudin-18, E- cadherin, and junction adhesion molecule (JAM)-A, and stabilization of zonula occludens (ZO)-1 at junction complexes. The Epac/Rap1 pathway was observed to play a role in the ECM-mediated barrier function determined by protein expression and Epac inhibition. These findings reveal potential ECM coatings and molecular therapeutic targets for improved regeneration with decellularized scaffolds or edema related pathologies.

scholarly journals Chymase-mediated intestinal epithelial permeability is regulated by a protease-activating receptor/matrix metalloproteinase-2-dependent mechanism

2013 ◽  
Vol 304 (5) ◽  
pp. G479-G489 ◽  
Author(s):  
Katherine R. Groschwitz ◽  
David Wu ◽  
Heather Osterfeld ◽  
Richard Ahrens ◽  
Simon P. Hogan
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Epithelial Barrier Dysfunction

Mast cells regulate intestinal barrier function during disease and homeostasis. Secretion of the mast cell-specific serine protease chymase regulates homeostasis. In the present study, we employ in vitro model systems to delineate the molecular pathways involved in chymase-mediated intestinal epithelial barrier dysfunction. Chymase stimulation of intestinal epithelial (Caco-2 BBe) cell monolayers induced a significant reduction in transepithelial resistance, indicating decreased intestinal epithelial barrier function. The chymase-induced intestinal epithelial barrier dysfunction was characterized by chymase-induced protease-activated receptor (PAR)-2 activation and matrix metalloproteinase (MMP)-2 expression and activation. Consistent with this observation, in vitro analysis revealed chymase-induced PAR-2 activation and increased MAPK activity and MMP-2 expression. Pharmacological and small interfering RNA-mediated antagonism of PAR-2 and MMP-2 significantly attenuated chymase-stimulated barrier dysfunction. Additionally, the chymase/MMP-2-mediated intestinal epithelial dysfunction was associated with a significant reduction in the tight junction protein claudin-5, which was partially restored by MMP-2 inhibition. Finally, incubation of Caco-2 BBe cells with chymase-sufficient, but not chymase-deficient, bone marrow-derived mast cells decreased barrier function, which was attenuated by the chymase inhibitor chymostatin. Collectively, these results suggest that mast cell/chymase-mediated intestinal epithelial barrier function is mediated by PAR-2/MMP-2-dependent pathways.

scholarly journals Acidic Bile Salt Modulates the Squamous Epithelial Barrier Function by Modulating Tight Junction Protein

2011 ◽  
Vol 140 (5) ◽  
pp. S-619-S-620
Author(s):  
Xin Chen ◽  
Tadayuki Oshima ◽  
Toshihiko Tomita ◽  
Hirokazu Fukui ◽  
Jiro Watari ◽  
...  
Keyword(s):  
Tight Junction ◽  
Bile Salt ◽  
Barrier Function ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Junction Protein

scholarly journals Lubiprostone Induces Claudin-1 and Protects Intestinal Barrier Function

Pharmacology ◽  
2019 ◽  
Vol 105 (1-2) ◽  
pp. 102-108 ◽  
Author(s):  
Norio Nishii ◽  
Tadayuki Oshima ◽  
Min Li ◽  
Hirotsugu Eda ◽  
Kumiko Nakamura ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Barrier ◽  
Fluorescein Isothiocyanate ◽  
Intestinal Barrier Function ◽  
Epithelial Barrier ◽  
Dependent Manner ◽  
Epithelial Permeability ◽  
Epithelial Barrier Function ◽  
Dose Dependent

Introduction: Lubiprostone, a chloride channel activator, is said to reduce epithelial permeability. However, whether lubiprostone has a direct effect on the epithelial barrier function and how it modulates the intestinal barrier function remain unknown. Therefore, the effects of lubiprostone on intestinal barrier function were evaluated in vitro. Methods: Caco-2 cells were used to assess the intestinal barrier function. To examine the expression of claudins, immunoblotting was performed with specific antibodies. The effects of lubiprostone on cytokines (IFNγ, IL-6, and IL-1β) and aspirin-induced epithelial barrier disruption were assessed by transepithelial electrical resistance (TEER) and fluorescein isothiocyanate (FITC) labeled-dextran permeability. Results: IFNγ, IL-6, IL-1β, and aspirin significantly decreased TEER and increased epithelial permeability. Lubiprostone significantly improved the IFNγ-induced decrease in TEER in a dose-dependent manner. Lubiprostone significantly reduced the IFNγ-induced increase in FITC labeled-dextran permeability. The changes induced by IL-6, IL-1β, and aspirin were not affected by lubiprostone. The expression of claudin-1, but not claudin-3, claudin-4, occludin, and ZO-1 was significantly increased by lubiprostone. Conclusion: Lubiprostone significantly improved the IFNγ-induced decrease in TEER and increase in FITC labeled-dextran permeability. Lubiprostone increased the expression of claudin-1, and this increase may be related to the effect of lubiprostone on the epithelial barrier function.

scholarly journals Role of JAM-A tyrosine phosphorylation in epithelial barrier dysfunction during intestinal inflammation

2019 ◽  
Vol 30 (5) ◽  
pp. 566-578 ◽  
Author(s):  
Shuling Fan ◽  
Caroline M. Weight ◽  
Anny-Claude Luissint ◽  
Roland S. Hilgarth ◽  
Jennifer C. Brazil ◽  
...  
Keyword(s):  
Tyrosine Phosphorylation ◽  
Barrier Function ◽  
Intestinal Inflammation ◽  
Kinase Inhibitor ◽  
Src Kinase ◽  
Small Gtpase ◽  
Epithelial Barrier ◽  
Barrier Dysfunction ◽  
Junction Protein

Junctional adhesion molecule-A (JAM-A), an epithelial tight junction protein, plays an important role in regulating intestinal permeability through association with a scaffold signaling complex containing ZO-2, Afadin, and the small GTPase Rap2. Under inflammatory conditions, we report that the cytoplasmic tail of JAM-A is tyrosine phosphorylated (p-Y280) in association with loss of barrier function. While barely detectable Y280 phosphorylation was observed in confluent monolayers of human intestinal epithelial cells under basal conditions, exposure to cytokines TNFα, IFNγ, IL-22, or IL-17A, resulted in compromised barrier function in parallel with increased p-Y280. Phosphorylation was Src kinase dependent, and we identified Yes-1 and PTPN13 as a major kinase and phosphatase for p-JAM-A Y280, respectively. Moreover, cytokines IL-22 or IL-17A induced increased activity of Yes-1. Furthermore, the Src kinase inhibitor PP2 rescued cytokine-induced epithelial barrier defects and inhibited phosphorylation of JAM-A Y280 in vitro. Phosphorylation of JAM-A Y280 and increased permeability correlated with reduced JAM-A association with active Rap2. Finally, we observed increased phosphorylation of Y280 in colonic epithelium of individuals with ulcerative colitis and in mice with experimentally induced colitis. These findings support a novel mechanism by which tyrosine phosphorylation of JAM-A Y280 regulates epithelial barrier function during inflammation.

scholarly journals The role of secreted Hsp90α in HDM-induced asthmatic airway epithelial barrier dysfunction

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Cuiping Ye ◽  
Chaowen Huang ◽  
Mengchen Zou ◽  
Yahui Hu ◽  
Lishan Luo ◽  
...  
Keyword(s):  
Barrier Function ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Function ◽  
Asthmatic Airway ◽  
Epithelial Barrier Dysfunction

Abstract Background The dysfunction of airway epithelial barrier is closely related to the pathogenesis of asthma. Secreted Hsp90α participates in inflammation and Hsp90 inhibitor protects endothelial dysfunction. In the current study, we aimed to explore the role of secreted Hsp90α in asthmatic airway epithelial barrier function. Methods Male BALB/c mice were sensitized and challenged with HDM to generate asthma model. The 16HBE and Hsp90α-knockdown cells were cultured and treated according to the experiment requirements. Transepithelial Electric Resistance (TEER) and permeability of epithelial layer in vitro, distribution and expression of junction proteins both in vivo and in vitro were used to evaluate the epithelial barrier function. Western Blot was used to evaluate the expression of junction proteins and phosphorylated AKT in cells and lung tissues while ELISA were used to evaluate the Hsp90α expression and cytokines release in the lung homogenate. Results HDM resulted in a dysfunction of airway epithelial barrier both in vivo and in vitro, paralleled with the increased expression and release of Hsp90α. All of which were rescued in Hsp90α-knockdown cells or co-administration of 1G6-D7. Furthermore, either 1G6-D7 or PI3K inhibitor LY294002 suppressed the significant phosphorylation of AKT, which caused by secreted and recombinant Hsp90α, resulting in the restoration of epithelial barrier function. Conclusions Secreted Hsp90α medicates HDM-induced asthmatic airway epithelial barrier dysfunction via PI3K/AKT pathway, indicating that anti-secreted Hsp90α therapy might be a potential treatment to asthma in future.

scholarly journals Diesel Exhaust Particle Exposure Reduces Expression of the Epithelial Tight Junction Protein Tricellulin

2020 ◽  
Author(s):  
Timothy Smyth ◽  
Janelle Veazey ◽  
Sophia Eliseeva ◽  
David Chalupa ◽  
Alison Elder ◽  
...  
Keyword(s):  
Tight Junction ◽  
Diesel Exhaust ◽  
Barrier Function ◽  
Diesel Exhaust Particles ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Epithelial Barrier Function ◽  
Barrier Integrity ◽  
Junction Protein

Abstract Background: While exposure to diesel exhaust particles has been linked to aberrant immune responses in allergic diseases such as asthma, little attention has been paid to their effects on the airway epithelium. In this study, we sought to determine the effect of diesel exhaust exposure on airway epithelial barrier function and composition using in vitro and in vivo model systems. Methods: 16HBE14o- human bronchial epithelial cells were grown on collagen coated Transwell inserts and exposed to 5 to 50 µg/cm2 SRM 2975 diesel particulate matter (DEP) suspended in cell culture medium or vehicle controls. Changes in barrier function were assessed by measuring transepithelial electrical resistance (TEER) and permeability to 4 kDa FITC Dextran. Neonatal BALB/c mice were exposed to aerosolized DEP (255 ± 89 µg/m3; 2 hours per day for 5 days) and changes in the tight junction protein Tricellulin were assessed two weeks post exposure. Results: A six-hour incubation of epithelial cells with diesel exhaust particles caused a significant concentration-dependent reduction in epithelial barrier integrity as measured by decreased TEER and increased permeability to 4 kDa FITC-Dextran. This reduction in epithelial barrier integrity corresponded to a significant reduction in expression of the tight junction protein Tricellulin. siRNA mediated knockdown of Tricellulin recapitulated changes in barrier function caused by DEP exposure. Neonatal exposure to aerosolized DEP caused a significant reduction in lung Tricellulin two weeks post exposure at both the protein and mRNA level. Conclusion: Short term exposure to DEP causes a significant reduction in epithelial barrier integrity through a reduction in the tight junction protein Tricellulin. Neonatal exposure to aerosolized DEP caused a significant and sustained reduction in Tricellulin protein and mRNA in the lung, suggesting that early life exposure to inhaled DEP may cause lasting changes in airway epithelial barrier function.

scholarly journals Diesel Exhaust Particle Exposure Reduces Expression of the Epithelial Tight Junction Protein Tricellulin

2020 ◽  
Author(s):  
Timothy Smyth ◽  
Janelle Veazey ◽  
Sophia Eliseeva ◽  
David Chalupa ◽  
Alison Elder ◽  
...  
Keyword(s):  
Tight Junction ◽  
Diesel Exhaust ◽  
Barrier Function ◽  
Diesel Exhaust Particles ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Epithelial Barrier Function ◽  
Barrier Integrity ◽  
Junction Protein

Abstract Background While exposure to diesel exhaust particles has been linked to aberrant immune responses in allergic diseases such as asthma, little attention has been payed to their effects on the airway epithelium. In this study, we sought to determine the effect of diesel exhaust exposure on airway epithelial barrier function and composition using in vitro and in vivo model systems. 16HBE14o- human bronchial epithelial cells were grown on collagen coated Transwell inserts and exposed to 5 to 50 µg/cm2 SRM 2975 diesel particulate matter (DEP) suspended in cell culture medium or vehicle controls. Changes in barrier function were assessed by measuring transepithelial electrical resistance (TEER) and permeability to 4 kDa FITC Dextran. Neonatal BALB/c mice were exposed to aerosolized DEP (255 ± 89 µg/m3; 2 hours per day for 5 days) and changes in the tight junction protein Tricellulin were assessed two weeks post exposure. Results A six-hour incubation of epithelial cells with diesel exhaust particles caused a significant concentration-dependent reduction in epithelial barrier integrity as measured by decreased TEER and increased permeability to 4 kDa FITC-Dextran. This reduction in epithelial barrier integrity corresponded to a significant reduction in expression of the tight junction protein Tricellulin. siRNA mediated knockdown of Tricellulin recapitulated changes in barrier function caused by DEP exposure. Neonatal exposure to aerosolized DEP caused a significant reduction in lung Tricellulin two weeks post exposure at both the protein and mRNA level. Conclusion Short term exposure to DEP causes a significant reduction in epithelial barrier integrity through a reduction in the tight junction protein Tricellulin. Neonatal exposure to aerosolized DEP caused a significant and sustained reduction in Tricellulin protein and mRNA in the lung, suggesting that early life exposure to inhaled DEP may cause lasting changes in airway epithelial barrier function.

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