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.

Flavonoids stimulate Cl conductance of human airway epithelium in vitro and in vivo.

Abstract: The ability of the flavonoids genistein, apigenin, kaempferol, and quercetin to activate cystic fibrosis transmembrane conductance regulator-mediated Cl currents in human airway epithelium was inve...

In vivo effects of endotoxin on intraepithelial mucosubstances in rat pulmonary airways. Quantitative histochemistry.

Abstract: Bacteria-induced bronchopneumonias are often characterized by an influx of neutrophils and excess mucus in pulmonary airways This study determined how endotoxin, a component of gram-negative bacteria and a potent inflammatory agent, affects the ultrastructure of the mucociliary apparatus and the amount of stored intraepithelial mucosubstances in the main axial airways within the lung Rats were intranasally instilled, once a day for 3 days, with endotoxin or saline (controls) Animals were sacrificed 1, 2, or 7 days after the last instillation Microdissected intrapulmonary axial airways (generations 8-11) from the right caudal lobes of infusion-fixed lungs were processed for light and electron microscopy Morphometric techniques were used to determine the volume densities (Vs) of histochemically stained intraepithelial mucosubstances and numerical densities of airway epithelial cells There were marked increases, compared with controls, in the amount of intraepithelial mucosubstances in the intrapulmonary axial airways at generations 8 and 11 in the right caudal lobes from endotoxin-instilled rats sacrificed 1, 2, and 7 days after the last instillation There were significantly greater numbers of surface epithelial cells per length of basal lamina (ie, hyperplasia) in endotoxin-exposed airways compared with airways from controls This endotoxin-induced hyperplasia was due primarily to an increase in the number of mucus-secretory cells, which in endotoxin-exposed epithelium were columnar and contained numerous, large confluent, electronlucent, secretory granules composed of acidic and neutral glycoproteins In contrast, secretory cells in airway epithelium from controls were cuboidal and contained small discrete, electron-dense, granules composed of only neutral glycoproteins The numbers of ciliated cells and basal cells were similar in both control and endotoxin-exposed epithelium Only endotoxin-exposed epithelium, however, contained atypical epithelial cells with numerous basal bodies, few cilia, and few apical secretory granules These results indicate that repeated airway instillations of endotoxin induce an increase in the amount of intraepithelial mucosubstances, secretory cell hyperplasia, and excess luminal mucus in pulmonary airways Therefore, endotoxin released from gram-negative bacteria may be partially responsible for the structural alterations, in the airway surface epithelium, which result in the excess luminal mucus observed in bacteria-induced bronchopneumonias

Chronic Respiratory Aeroallergen Exposure in Mice Induces Epithelial-Mesenchymal Transition in the Large Airways

Abstract: Chronic allergic asthma is characterized by Th2-polarized inflammation and leads to airway remodeling and fibrosis but the mechanisms involved are not clear. To determine whether epithelial-mesenchymal transition contributes to airway remodeling in asthma, we induced allergic airway inflammation in mice by intranasal administration of house dust mite (HDM) extract for up to 15 consecutive weeks. We report that respiratory exposure to HDM led to significant airway inflammation and thickening of the smooth muscle layer in the wall of the large airways. Transforming growth factor beta-1 (TGF-β1) levels increased in mouse airways while epithelial cells lost expression of E-cadherin and occludin and gained expression of the mesenchymal proteins vimentin, alpha-smooth muscle actin (α-SMA) and pro-collagen I. We also observed increased expression and nuclear translocation of Snail1, a transcriptional repressor of E-cadherin and a potent inducer of EMT, in the airway epithelial cells of HDM-exposed mice. Furthermore, fate-mapping studies revealed migration of airway epithelial cells into the sub-epithelial regions of the airway wall. These results show the contribution of EMT to airway remodeling in chronic asthma-like inflammation and suggest that Th2-polarized airway inflammation can trigger invasion of epithelial cells into the subepithelial regions of the airway wall where they contribute to fibrosis, demonstrating a previously unknown plasticity of the airway epithelium in allergic airway disease.