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Open AccessJournal ArticleDOI

Barrier function of airway tract epithelium

TLDR
In this paper, the authors reviewed the regulation of components of barrier function with respect to chronic airway diseases and showed that impairment of one or more of these essential components may increase susceptibility to infection and promote exaggerated and prolonged innate immune responses to environmental factors including allergens and pathogens resulting in chronic inflammation.
Abstract
Airway epithelium contributes significantly to the barrier function of airway tract. Mucociliary escalator, intercellular apical junctional complexes which regulate paracellular permeability and antimicrobial peptides secreted by the airway epithelial cells are the three primary components of barrier function of airway tract. These three components act cooperatively to clear inhaled pathogens, allergens and particulate matter without inducing inflammation and maintain tissue homeostasis. Therefore impairment of one or more of these essential components of barrier function may increase susceptibility to infection and promote exaggerated and prolonged innate immune responses to environmental factors including allergens and pathogens resulting in chronic inflammation. Here we review the regulation of components of barrier function with respect to chronic airways diseases.

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Citations
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Pathogens Penetrating the Central Nervous System: Infection Pathways and the Cellular and Molecular Mechanisms of Invasion

TL;DR: Recent data regarding mechanisms of bacterial translocation from the nasal mucosa to the brain are focused on, which represents a little explored pathway of bacterial invasion but has been proposed as being particularly important in explaining how infection with Burkholderia pseudomallei can result in melioidosis encephalomyelitis.
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Antimicrobial peptides and wound healing: biological and therapeutic considerations

TL;DR: The evidence for a role of AMPs as endogenous mediators of wound healing and their promising therapeutic potential for the treatment of non‐life‐threatening skin and other epithelial injuries is provided.
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The cell biology of asthma

TL;DR: The clinical manifestations of asthma are caused by obstruction of the conducting airways of the lung as mentioned in this paper, and two airway cell types are critical for asthma pathogenesis: epithelial cells and smooth muscle cells.
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The Interaction between Respiratory Pathogens and Mucus.

TL;DR: This review summarizes the current understanding of respiratory mucus and its interactions with the respiratory pathogens Pseudomonas aeruginosa, respiratory syncytial virus and influenza viruses, with particular focus on influenza virus transmissibility and host-range specificity.
Journal ArticleDOI

Airway Epithelial Barrier Dysfunction in Chronic Obstructive Pulmonary Disease: Role of Cigarette Smoke Exposure

TL;DR: Recent advances in understanding the mechanisms of barrier dysfunction in COPD are discussed, as well as the molecular mechanisms that underlie the impaired repair response of the injured epithelium and its inability to redifferentiate into a functionally intact epithelia.
References
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Journal ArticleDOI

Isolation of a Common Receptor for Coxsackie B Viruses and Adenoviruses 2 and 5

TL;DR: Identification of CAR as a receptor for these two unrelated and structurally distinct viral pathogens is important for understanding viral pathogenesis and has implications for therapeutic gene delivery with adenovirus vectors.
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Defensins: antimicrobial peptides of innate immunity.

TL;DR: This review, inspired by a spate of recent studies ofdefensins in human diseases and animal models, focuses on the biological function of defensins.
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Interleukin-13: Central Mediator of Allergic Asthma

TL;DR: In this paper, the type 2 cytokine IL-13, which shares a receptor component and signaling pathways with IL-4, was found to be necessary and sufficient for the expression of allergic asthma.
Journal Article

Interleukin-13: Central mediator of allergic asthma

TL;DR: In this article, the type 2 cytokine IL-13, which shares a receptor component and signaling pathways with IL-4, was found to be necessary and sufficient for the expression of allergic asthma.
Journal ArticleDOI

Requirement for IL-13 Independently of IL-4 in Experimental Asthma

TL;DR: This article showed that IL-4 receptor α chain-dependent pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL4 receptor and showed that selective neutralization of IL-13, a cytokine related to interleukin-4 that also binds to the α chain of the IL 4 receptor, ameliorated asthma phenotype.
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