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.

Visualization of in vivo olfactory uptake and transfer using fluorescein dextran.

Abstract: Nasal administration of a 3 kDa fluorescein dextran (FD3) solution to rats resulted in transcellular absorption across the olfactory epithelium and transfer to the olfactory bulb within 15 min. After entering the lamina propria, FD3 was transferred in the connective tissue surrounding the olfactory nerve bundles to the olfactory bulb of the brain. More FD3 was absorbed across the olfactory epithelium than across the respiratory epithelium and to the nasal associated lymphoid tissue. Further, the amount of FD3 crossing the olfactory epithelium was region-dependent, with higher amounts absorbed in the turbinates than in the nasal septum. Plastic embedding and sectioning followed by fluorescence microscopy, enabled simultaneous visualization of FD3 in the mucosa and olfactory bulb, as well as the opportunity to store the tissue blocks for a prolonged period of time.

Expression of phenotypic markers during regeneration of rat tracheal epithelium following mechanical injury.

Abstract: We examined epithelial regeneration in mechanically injured rat trachea using phenotypic markers that identify unique differentiated stages of epithelial cells. Following a focal denuding wound, the cells from the adjacent nonwounded epithelium flattened and migrated into the wounded site during the first 12 h. At 24 h, these cells dedifferentiated into poorly differentiated (PD) cells that did not precisely resemble any of the mature tracheal cells. Proliferation of PD cells produced a multilayered epithelium by 48 h. Mitotic activity, measured as mitotic rate (MR) following a 6-h colchicine metaphase blockade, was high at 24 h (MR 23.4%) and 48 h (MR 24.0%). These PD cells expressed keratin 14 and Griffonia simplicifolia I-isolectin B4 (GSI-B4) lectin binding sites, which are specific for basal cells in normal epithelium but did not react with secretory or ciliated cell markers. At 72 h, MR fell to 1.8% (control MR 0.38%). The wound was covered with a pseudostratified epithelium; secretory cell markers ...

Effects of TNF-alpha, IFN-gamma and IL-beta on normal human bronchial epithelial cells

Abstract: Several diseases affecting the airways such as asthma are associated with both epithelial damage and increased levels of pro-inflammatory cytokines. To investigate the possible relation between cytokines and epithelial damage, the effects of tumour necrosis factor-alpha (TNF)-alpha, interferon gamma (IFN-gamma) and interleukin-1 beta (IL-1beta) on normal human bronchial epithelial cells in vitro were studied. The cells were exposed to these cytokines for 48 or 72 h, followed by morphological, immunohistochemical and metabolic studies. Transmission and scanning electron microscopical analyses demonstrated damage to the mitochondria and an increase in cell processes induced by the cytokines. The use of antibodies against desmosomal cytokeratin showed a decrease in desmosome formation in IFN-gamma-exposed cells. Decreased glucose oxidation rate and increased accumulation of nitric oxide were found in cytokine-exposed cells. Nomega-monomethyl-L-arginine (L-NMMA) reduced nitrite production. X-ray microanalysis showed an increase in the intracellular sodium/potassium ratio of the cells after exposure to cytokines, which is an indication of cell damage. The cytokines induced both necrosis and apoptosis to varying degrees. IFN-gamma and TNF-alpha generally potentiate each other's effects. In conclusion tumour necrosis factor-alpha and interferon gamma, and to a lesser extent interleukin-1beta, can cause damage to epithelial cells, which may be a factor involved in epithelial shedding in airway diseases.

Stimulation of Cl− Secretion by Chlorzoxazone

Abstract: We previously demonstrated that 1-ethyl-2-benzimidazolone (1-EBIO) directly activates basolateral membrane calcium-activated K+ channels (KCa), thereby stimulating Cl− secretion across several epithelia. In our pursuit to identify potent modulators of Cl− secretion that may be useful to overcome the Cl− secretory defect in cystic fibrosis (CF), we have identified chlorzoxazone [5-chloro-2(3H)-benzoxazolone], a clinically used centrally acting muscle relaxant, as a stimulator of Cl− secretion in several epithelial cell types, including T84, Calu-3, and human bronchial epithelium. The Cl− secretory response induced by chlorzoxazone was blocked by charybdotoxin (CTX), a known blocker of KCa. In nystatin-permeabilized monolayers, chlorzoxazone stimulated a basolateral membrane I K, which was inhibited by CTX and also stimulated an apical I Cl that was inhibited by glibenclamide, indicating that the G Cl responsible for this I Cl may be cystic fibrosis transmembrane conductance regulator (CFTR). In membrane vesicles prepared from T84 cells, chlorzoxazone stimulated 86Rb+ uptake in a CTX-sensitive manner. In excised, inside-out patches, chlorzoxazone activated an inwardly-rectifying K+ channel, which was inhibited by CTX. 6-Hydroxychlorzoxazone, the major metabolite of chlorzoxazone, did not activate KCa, whereas zoxazolamine (2-amino-5-chlorzoxazole) showed a similar response profile as chlorzoxazone. In normal human nasal epithelium, chlorzoxazone elicited hyperpolarization of the potential difference that was similar in magnitude to isoproterenol. However, in the nasal epithelium of CF patients with the ΔF508 mutation of CFTR, there was no detectable Cl− secretory response to chlorzoxazone. These studies demonstrate that chlorzoxazone stimulates transepithelial Cl− secretion in normal airway epithelium in vitro and in vivo, and suggest that stimulation requires functional CFTR in the epithelia.