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Respiratory epithelium

About: Respiratory epithelium is a research topic. Over the lifetime, 5048 publications have been published within this topic receiving 222304 citations. The topic is also known as: respiratory tract epithelium & Respiratory Mucosa.


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Journal ArticleDOI
TL;DR: The regulation of Duox expression by immunomodulatory Th1 and Th2 cytokines is demonstrated for the first time, and a mechanism by which ROS production can be regulated in the respiratory tract as part of the host defense response is suggested.

236 citations

Journal ArticleDOI
TL;DR: This review provides an update on the current understanding of how shear stress regulates ASL volume height in normal and cystic fibrosis (CF) airway epithelia through extracellular ATP- and adenosine (ADO)-mediated pathways that modulate ion transport and ASLVolume homeostasis.
Abstract: The physical removal of viruses and bacteria on the mucociliary escalator is an important aspect of the mammalian lung's innate defense mechanism. The volume of airway surface liquid (ASL) present in the respiratory tract is a critical determinant of both mucus hydration and the rate of mucus clearance from the lung. ASL volume is maintained by the predominantly ciliated epithelium via coordinated regulation of (a) absorption, by the epithelial Na+ channel, and (b) secretion, by the Ca2+-activated Cl- channel (CaCC) and CFTR. This review provides an update on our current understanding of how shear stress regulates ASL volume height in normal and cystic fibrosis (CF) airway epithelia through extracellular ATP- and adenosine (ADO)-mediated pathways that modulate ion transport and ASL volume homeostasis. We also discuss (a) how derangement of the ADO-CFTR pathway renders CF airways vulnerable to viral infections that deplete ASL volume and produce mucus stasis, and (b) potential shear stress-dependent therapies for CF.

236 citations

Journal ArticleDOI
TL;DR: The data demonstrate that an Ad vector can deliver sufficient levels of CFTR cDNA to the airway epithelium so that CFTR expression protects the lungs from the respiratory manifestations of CF, and further repetitive administration does not lead to repetitive expression.
Abstract: We sought to evaluate the ability of an E1(-), E3(-) adenovirus (Ad) vector (Ad(GV)CFTR.10) to transfer the normal human cystic fibrosis transmembrane conductance regulator (CFTR) cDNA to the airway epithelium of individuals with cystic fibrosis (CF). We administered Ad(GV)CFTR.10 at doses of 3 x 10(6) to 2 x 10(9) plaque-forming units over 9 months by endobronchial spray to 7 pairs of individuals with CF. Each 3-month cycle, we measured vector-derived versus endogenous CFTR mRNA in airway epithelial cells prior to therapy, as well as 3 and 30 days after therapy. The data demonstrate that (a) this strategy appears to be safe; (b) after the first administration, vector-derived CFTR cDNA expression in the CF airway epithelium is dose-dependent, with greater than 5% endogenous CFTR mRNA levels at the higher vector doses; (c) expression is transient, lasting less than 30 days; (d) expression can be achieved with a second administration, but only at intermediate doses, and no expression is observed with the third administration; and (e) the progressive lack of expression with repetitive administration does not closely correlate with induction of systemic anti-Ad neutralizing antibodies. The major advantage of an Ad vector is that it can deliver sufficient levels of CFTR cDNA to the airway epithelium so that CFTR expression protects the lungs from the respiratory manifestations of CF. However, this impressive level of expression is linked to the challenging fact that expression is limited in time. Although this can be initially overcome by repetitive administration, unknown mechanisms eventually limit this strategy, and further repetitive administration does not lead to repetitive expression.

236 citations

Journal ArticleDOI
TL;DR: Observations suggest that MMP-9 controls the migration of repairing HBEC by remodeling the provisional ECM implicated in primordial contacts, which is involved in cell migration.
Abstract: Cell spreading and migration associated with the expression of the 92-kD gelatinase (matrix metalloproteinase 9 or MMP-9) are important mechanisms involved in the repair of the respiratory epithelium. We investigated the location of MMP-9 and its potential role in migrating human bronchial epithelial cells (HBEC). In vivo and in vitro, MMP-9 accumulated in migrating HBEC located at the leading edge of a wound and MMP-9 expression paralleled cell migration speed. MMP-9 accumulated through an actin-dependent pathway in the advancing lamellipodia of migrating cells and was subsequently found active in the extracellular matrix (ECM). Lamellipodia became anchored through primordial contacts established with type IV collagen. MMP-9 became amassed behind collagen IV where there were fewer cell–ECM contacts. Both collagen IV and MMP-9 were involved in cell migration because when cell–collagen IV interaction was blocked, cells spread slightly but did not migrate; and when MMP-9 activation was prevented, cells remained fixed on primordial contacts and did not advance at all. These observations suggest that MMP-9 controls the migration of repairing HBEC by remodeling the provisional ECM implicated in primordial contacts.

235 citations

Journal ArticleDOI
TL;DR: These intrinsic antimicrobial properties of respiratory secretions act in concert with the mechanical and phagocytic clearance mechanisms, described elsewhere in this Perspective series, to defend the respiratory tract against colonization or invasion by environmental microbes.
Abstract: The large surfaces of the respiratory tract are often the initial site of contact between microbes and their human hosts. Respiratory epithelia are coated with a thin layer of airway and alveolar secretions whose composition varies by anatomical location and in response to mechanical, chemical, and microbial stimulation. In the nose, trachea, and bronchi, the secretions are generated by airway epithelial cells, especially the goblet cells; by the submucosal glands; by transudation and transport of proteins from plasma; and by resident and recruited phagocytes — neutrophils, eosinophils, monocytes, and macrophages. In the distal airways and alveoli, Clara cells and type 2 alveolar cells are, respectively, the predominant secretory epithelial cells. As first described by Alexander Fleming nearly 80 years ago (1), respiratory secretions have microbicidal and microbistatic properties mediated by their constituent antimicrobial polypeptides. These intrinsic antimicrobial properties of respiratory secretions act in concert with the mechanical and phagocytic clearance mechanisms, described elsewhere in this Perspective series, to defend the respiratory tract against colonization or invasion by environmental microbes.

233 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023143
2022222
2021182
2020174
2019149
2018149