Sieving characteristics of cytokine- and peroxide-induced epithelial barrier leak: Inhibition by berberine

DiGuilio, Katherine M; Mercogliano, Christina; Born, Jillian; Ferraro, Brendan; To, Julie; Mixson, Brittany; Smith, Allison; Valenzano, Mary Carmen; Mullin, James M.

doi:10.4291/wjgp.v7.i2.223

Cited by 17 publications

(13 citation statements)

References 42 publications

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“…TJ-dependent paracellular passages manage the exchange of paracellular substances between the intestinal lumen and internal environment, thereby playing a role in the balancing of nutrient absorption and waste secretion as well as defense mechanisms against pathogens. In accordance with the well-acknowledged roles of claudins in forming TJs and selective channels, claudins may participate in both types of transepithelial paracellular leakage (25): proinflammatory cytokines-induced small molecule (e.g., ions and mannitol) channel disruption and cell detachment-induced large molecule (e.g., epidermal growth factor, EGF) leakage (26). Thus, as barrier-forming proteins, dysregulated expression and redistribution of claudins may lead to increased intestinal permeability, susceptibility to gut infection and bowel symptoms of IBD patients (27–29).…”

Section: Pathogenesis Of Ibdmentioning

confidence: 90%

Claudin Family Participates in the Pathogenesis of Inflammatory Bowel Diseases and Colitis-Associated Colorectal Cancer

Zhu

Han

et al. 2019

Front. Immunol.

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Claudins are a multigene transmembrane protein family comprising at least 27 members. In gastrointestinal tract, claudins are mainly located in the intestinal epithelia; many types of claudins form a network of strands in tight junction plaques within the intercellular space of neighboring epithelial cells and build paracellular selective channels, while others act as signaling proteins and mediates cell behaviors. Claudin dysfunction may contribute to epithelial permeation disorder and multiple intestinal diseases. Over recent years, the importance of claudins in the pathogenesis of inflammatory bowel diseases (IBD) has gained focus and is being investigated. This review analyzes the expression pattern and regulatory mechanism of claudins based on existing evidence and elucidates the fact that claudin dysregulation correlates with increased intestinal permeability, sustained activation of inflammation, epithelial-to-mesenchymal transition (EMT), and tumor progression in IBD as well as consequent colitis-associated colorectal cancer (CAC), possibly shedding new light on further etiologic research and clinical treatments.

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Section: Pathogenesis Of Ibdmentioning

confidence: 90%

Claudin Family Participates in the Pathogenesis of Inflammatory Bowel Diseases and Colitis-Associated Colorectal Cancer

Zhu

Han

et al. 2019

Front. Immunol.

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“…TNF-α has been shown to produce barrier leak in a variety of other different epithelial cell models [6,26,[38][39][40][41][42][43]. The purpose of this study-with respect to TNF-α-induced barrier leak -was not to delve into the molecular mechanisms of how TNF-α produces leak in 16HBE cell layers, but rather initially characterize the type of leak that occurs.…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid improves baseline barrier function and attenuates TNF-α-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o-

et al. 2020

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Retinoic acid (RA) has been shown to improve epithelial and endothelial barrier function and development and even suppress damage inflicted by inflammation on these barriers through regulating immune cell activity. This paper thus sought to determine whether RA could improve baseline barrier function and attenuate TNF-α-induced barrier leak in the human bronchial epithelial cell culture model, 16HBE14o- (16HBE). We show for the first time that RA increases baseline barrier function of these cell layers indicated by an 89% increase in transepithelial electrical resistance (TER) and 22% decrease in 14C-mannitol flux. A simultaneous, RA-induced 70% increase in claudin-4 attests to RA affecting the tight junctional (TJ) complex itself. RA was also effective in alleviating TNF-α-induced 16HBE barrier leak, attenuating 60% of the TNF-α-induced leak to 14C-mannitol and 80% of the leak to 14C-inulin. Interleukin-6-induced barrier leak was also reduced by RA. Treatment of 16HBE cell layers with TNF-α resulted in dramatic decrease in immunostaining for occludin and claudin-4, as well as a downward “band-shift” in occludin Western immunoblots. The presence of RA partially reversed TNF-α’s effects on these select TJ proteins. Lastly, RA completely abrogated the TNF-α-induced increase in ERK-1,2 phosphorylation without significantly decreasing the TNF-driven increase in total ERK-1,2. This study suggests RA could be effective as a prophylactic agent in minimizing airway barrier leak and as a therapeutic in preventing leak triggered by inflammatory cascades. Given the growing literature suggesting a “cytokine storm” may be related to COVID-19 morbidity, RA may be a useful adjuvant for use with anti-viral therapies.

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“…From a wider perspective, GI barrier function also may be compromised by an impaired mucus layer over the epithelium (a topic reviewed nicely by others recently [Chen et al, (313)]), as well as by cell death in the epithelium or an epithelial-mesenchymal transition leading to impaired cell adhesion/attachment (to other cells and substratum). Leak at sites of compromised TJ may be quite distinct in nature from leak at sites of cell death (314). Likewise the remediation of leak is very different in these cases – repair of leak from impaired TJ may be a purely transcription/translation/phosphorylation-based process, whereas remediation of leak due to cell death/dedifferentiation/detachment could also require a careful orchestration of cell motility and cell replication.…”

Section: Microbiome Effects On Intestinal Barrier Function and Inflammentioning

confidence: 99%

The Host Microbiome Regulates and Maintains Human Health: A Primer and Perspective for Non-Microbiologists

et al. 2017

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Humans consider themselves discrete autonomous organisms, but recent research is rapidly strengthening the appreciation that associated microorganisms make essential contributions to human health and well-being. Each person is inhabited and also surrounded by his/her own signature microbial cloud. A low diversity of microorganisms is associated with a plethora of diseases including allergy, diabetes, obesity, arthritis, inflammatory bowel diseases and even neuropsychiatric disorders. Thus, an interaction of microorganisms with the host immune system is required for a healthy body. Exposure to microorganisms from the moment we are born and appropriate microbiome assembly during childhood are essential for establishing an active immune system necessary to prevent disease later in life. Exposure to microorganisms educates the immune system, induces adaptive immunity and initiates memory B and T cells that are essential to combat various pathogens. The correct microbial-based education of immune cells may be critical in preventing the development of autoimmune diseases and cancer. This review provides a broad overview of the importance of the host microbiome and accumulating knowledge of how it regulates and maintains a healthy human system.

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Sieving characteristics of cytokine- and peroxide-induced epithelial barrier leak: Inhibition by berberine

Abstract: This model of graded transepithelial leak is useful in evaluating therapeutic agents reducing IBD morbidity by reducing barrier leak to various luminal substances.

Cited by 17 publications

References 42 publications

Claudin Family Participates in the Pathogenesis of Inflammatory Bowel Diseases and Colitis-Associated Colorectal Cancer

Claudin Family Participates in the Pathogenesis of Inflammatory Bowel Diseases and Colitis-Associated Colorectal Cancer

Retinoic acid improves baseline barrier function and attenuates TNF-α-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o-

The Host Microbiome Regulates and Maintains Human Health: A Primer and Perspective for Non-Microbiologists

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