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.

The bone morphogenic protein antagonist gremlin regulates proximal-distal patterning of the lung.

Abstract: The proximal-distal patterning of lung epithelium involves a complex series of signaling and transcriptional events resulting in the programmed differentiation of highly specialized cells for gas exchange and surfactant protein expression essential for postnatal lung function. The BMP signaling pathway has been shown to regulate cellular differentiation in the lung as well as other tissues. In this report, we show that the can family of related BMP antagonists, including gremlin, cer-1, PRDC, and Dan are expressed in the lung during embryonic development with gremlin expression observed in the proximal airway epithelium. The role of gremlin in lung development was explored by overexpressing it in the distal lung epithelium of transgenic mice using the human SP-C promoter. SP-C/gremlin transgenic mice exhibited a disruption of the proximal-distal patterning found in the airways of the mammalian lung. Expanded expression of the proximal epithelial cell markers CC10 and HFH-4 (Foxj1) was observed in the distal regions of transgenic lungs. Furthermore, smooth muscle α-actin expression was observed surrounding the distal airways of SP-C/gremlin mice, indicating a proximalization of distal lung tubules. These data suggest that gremlin plays an important role in lung morphogenesis by regulating the proximal-distal patterning of the lung during development. © 2001 Wiley-Liss, Inc.

Biological characteristics of the junctional epithelium.

Abstract: This review summarizes the biological properties of the junctional epithelium, focusing on its developmental aspects, wide intercellular spaces and desmosomes, dense granules, permeability barrier, phagocytotic activity, adhesive structures and nerve terminals. It also discusses the morphology and functions of long junctional epithelium and peri-implant epithelium. Junctional epithelium is derived from the reduced enamel epithelium during tooth development. Apoptosis occurs in the border between oral and reduced enamel epithelia during tooth eruption. Junctional epithelium expresses a cytokeratin-19 immunoreaction, suggesting that this protein is a consistent differentiation marker. Wide intercellular spaces, which contain neutrophils and nerve endings, are formed as there are fewer desmosomes than in the oral epithelium. Dense, membrane-bound granules in the epithelium might correspond with membrane-coating granules, as revealed by their shape, components and freeze-fracture images. Junctional epithelium with high permeability contains exogenously expressed alpha-defensins, while stratified epithelia contain endogenously expressed beta-defensins. The phagocytotic activity in this epithelium remains unclear. Integrin-alpha6beta4 and laminin-5 form a complex in the tooth surface internal basal lamina. Long junctional epithelium created experimentally attaches to the cementum surface by hemidesmosomes and basal lamina. The peri-implant epithelium differs in proliferation and in adhesive structure from the normal junctional epithelium. In conclusion, wide intercellular spaces and poorly developed desmosomes are closely correlated with a permeable nature. There is still uncertainty over the phagocytotic activity of the epithelium. Integrin-alpha6beta4 and laminin-5 form a significant complex in the internal basal lamina. Junctional epithelium receives a rich sensory nerve and has a high rate of cell turnover. Long junctional epithelium can be produced rapidly during wound healing, due to high proliferative activity. Peri-implant epithelium might be a poorly adhered and permeable epithelium.

Glutathione aerosol suppresses lung epithelial surface inflammatory cell-derived oxidants in cystic fibrosis.

Abstract: Cystic fibrosis (CF) is characterized by accumulation of activated neutrophils and macrophages on the respiratory epithelial surface (RES); these cells release toxic oxidants, which contribute to t...

Moraxella catarrhalis is internalized in respiratory epithelial cells by a trigger-like mechanism and initiates a TLR2- and partly NOD1-dependent inflammatory immune response.

Abstract: Summary Moraxella catarrhalis is an important pathogen in patients with chronic obstructive lung disease (COPD). While M. catarrhalis has been categorized as an extracellular bacterium so far, the potential to invade human respiratory epithelium has not yet been explored. Our results obtained by electron and confocal microscopy demonstrated a considerable potential of M. catarrhalis to invade bronchial epithelial (BEAS-2B) cells, type II pneumocytes (A549) and primary small airway epithelial cells (SAEC). Moraxella invasion was dependent on cellular microfilament as well as on bacterial viability, and characterized by macropinocytosis leading to the formation of lamellipodia and engulfment of the invading organism into macropinosomes, thus indicating a trigger-like uptake mechanism. In addition, the cells examined expressed TLR2 as well as NOD1, a recently found cytosolic protein implicated in the intracellular recognition of bacterial cell wall components. Importantly, inhibition of TLR2 or NOD1 expression by RNAi significantly reduced the M. catarrhalis-induced IL-8 secretion. The role of TLR2 and NOD1 was further confirmed by overexpression assays in HEK293 cells. Overall, M. catarrhalis may employ lung epithelial cell invasion to colonize and to infect the respiratory tract, nonetheless, the bacteria are recognized by cell surface TLR2 and the intracellular surveillance molecule NOD1.

Nitric Oxide and Bronchial Hyperresponsiveness

Abstract: Increasing evidence points to an important role for nitric oxide (NO) in the regulation of pulmonary functions and in pulmonary disease [1, 2, 3, 4]. NO is present in exhaled air of animals and humans [1, 5]. The respiratory tract, nerves endothelial cells, vascular and airway smooth muscle cells, inflammatory cells (macrophages, neutrophils, mast cells) and the airway epithelium are sources for NO production [2]. The different effects of NO are mediated by the activation of soluble guanylyl cyclase, with as a consequence, an increase of cyclic guanosine monophosphate (cGMP) in the target cell.