Loss of Epithelial Integrity Resulting from E-Cadherin Dysfunction Predisposes Airway Epithelial Cells to Adenoviral Infection
Abstract
Epithelial intercellular adhesion is fundamental to the formation of the airway epithelial protective barrier. In this respect, cadherins are important because these adhesion molecules regulate formation and maintenance of epithelial intercellular junctions. To study the importance of airway epithelial integrity in determining susceptibility to virus infection, we used a replication-incompetent adenovirus, RAd35, and an E-cadherin specific function-blocking antibody, SHE78-7, to disrupt intercellular contacts in human bronchial epithelial cell line 16HBE14o- and primary bronchial epithelial cells. After exposure of 16HBE14o- cell cultures to SHE78-7, disruption of the transepithelial permeability barrier was indicated by a loss of transepithelial electrical resistance and an associated increase of mannitol, inulin, and dextran paracellular flux. Subsequent exposure of SHE78-7-treated cell cultures to RAd35 showed a remarkable increase in adenoviral infection as assessed by beta-galactosidase reporter gene expression. In cultures exposed to SHE78-7, disruption of E-cadherin function resulted in infection equivalent to that in control cultures using 16-fold lower viral titers. These studies show that manipulation of E-cadherin function provides a specific means of altering epithelial integrity that in turn determines resistance of airway epithelia to adenoviral infection.
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The sources and mechanisms of production of inflammatory mediators in gingival overgrowth tissues are unclear.
“However, currently, the sources and the mechanisms of the production of inflammatory mediators in the gingival overgrowth tissues are unclear [30].”
From An Update on the Mechanisms of Phenytoin Induced Gingival Overgrowth (2019) · cites this paper as [30]
Gingival sulcular tissue is more susceptible to the effects of phenytoin, causing gingival overgrowth.
“Thus, gingival sulcular tissue is more susceptible to the effects of phenytoin causing gingival overgrowth [ 30].”
From An Update on the Mechanisms of Phenytoin Induced Gingival Overgrowth (2019) · cites this paper as [30]
Phenytoin in saliva is absorbed or diffused via the sulcular epithelium into the serum, causing a double exposure to phenytoin via systemic circulation and saliva reabsorption.
“Phenytoin in the saliva is absorbed or diffused via the sulcular epithelium into the serum causing a double exposure to phenytoin via two pathways, mainly from the systemic circulation and partly from the reabsorption pathway of the saliva.”
From An Update on the Mechanisms of Phenytoin Induced Gingival Overgrowth (2019) · cites this paper as [30]
Phenytoin acts on macrophages, enhancing production of IL-1β, which enhances expression of COX-2 through NF-κB.
“Phenytoin acts on macrophages, enhancing the production of IL-1β, which enhances the expression of Cyclooxygenase 2 (COX-2) through the transcription factor (nuclear factorkappaB [NF-κB].”
From An Update on the Mechanisms of Phenytoin Induced Gingival Overgrowth (2019) · cites this paper as [30]
PGE-2 acts on EP-3 receptors in fibroblasts and enhances TGF-β1 stimulation of JNK-MAP kinase pathway of CTGF expression.
“PGE-2 acts on EP-3 receptors in fibroblasts and enhances the TGF-β1 stimulation of JNK -MAP kinase pathway of CTGF expression [30].”
From An Update on the Mechanisms of Phenytoin Induced Gingival Overgrowth (2019) · cites this paper as [30]
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Guo, X., Rao, J. N., Liu, L., Zou, T.-T., Turner, D. J., Bass, B. L., & Wang, J.-Y. (2003) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00015.2003 · Cited by 153 · see citing works
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Optimising non-viral gene delivery in a tumour spheroid model
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- Authors
- Man, Y., Hart, V. J., Ring, C. J. A., Sanjar, S., & West, M. R.
- Affiliations
- Cell Biology Department and Clinical Virology Department, Medicines Research Centre, GlaxoWellcome, Stevenage, United Kingdom; and Respiratory Therapeutic Development, GlaxoWellcome, Inc., Research Triangle Park, North Carolina
- Corresponding author
- Man, Yim
- Venue
- American Journal of Respiratory Cell and Molecular Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-11-01
- Volume
- 23
- Issue
- 5
- Pages
- 610-617
- ISSN
- 1044-1549 (ISSN-L)
- 1535-4989
- OpenAlex
- W1964585722
- Cited by
- 69
- References
- 0
- Citations by year
- 2024: 1 · 2023: 1 · 2020: 5 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 1 · 2015: 4 · 2014: 2 · 2013: 5 · 2012: 1
- FWCI
- 1.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Respiratory Cell and Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Virus-based gene therapy research
- Keywords
- E-cadherin, airway epithelial barrier, adenovirus infection, transepithelial permeability, epithelial junctions, viral susceptibility, bronchial epithelial cells
- MeSH terms
- Adenoviridae Infections, Adenoviruses, Human, Cell Communication, Cell Line, Epithelial Cells, Humans, Intercellular Junctions, Cadherins
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