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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: It is demonstrated that MECs can give rise to seven cell types of the SAE and SMGs following severe airway injury and modulating the Lef-1 transcriptional program in MEC-derived progenitors may have regenerative medicine applications for lung diseases.

89 citations

Journal ArticleDOI
TL;DR: Two major transmembranal polypeptides of bovine olfactory epithelium were identified by SDS electrophoretic analysis of Triton X-114 solubilized membranes and are consistent with a mechanism whereby the microsomal enzymes are involved in odorant modification and clearance from the nasal tissue.
Abstract: Two major transmembranal polypeptides of bovine olfactory epithelium were identified by SDS electrophoretic analysis of Triton X-114 solubilized membranes. Both polypeptides were present in large amounts in membranes of the olfactory epithelium but were barely detectable in membranes of the nasal respiratory epithelium. Both polypeptides are enriched in the deciliated epithelium as compared with isolated cilia. One of them is a glycoprotein with an apparent molecular mass of 56 kDa (gp56); the other is an unglycosylated protein with an apparent molecular mass of 52 kDa (p52). Sequence analysis of peptides obtained by CNBr cleavage of purified gp56 indicates that it is highly homologous to UDP-glucuronosyl transferase (UDPGT). Parallel analysis shows that p52 is highly homologous to cytochrome P-450 sequences of the IIA subfamily. This protein is assigned the name P-450olf2. Polyclonal antibodies were raised against synthetic peptides corresponding to gp56 and p52 peptide sequences. Immunoblots with these antibodies reveal the following properties of gp56 and p52: (1) they are enriched in the microsomal fraction of the bovine olfactory epithelium; (2) they are possibly specific to the olfactory epithelium, as we could not detect reactivity in microsomes derived from respiratory epithelium or lung, and only a very small amount of basal reactivity was seen with liver microsomes; (3) cross-reacting proteins exist in microsomes derived from the rat olfactory epithelium. These results are consistent with a mechanism whereby the microsomal enzymes are involved in odorant modification and clearance from the nasal tissue.

89 citations

Journal ArticleDOI
TL;DR: Rat foetuses from intra-uterine days E13 through E22 (day before parturition) and adults were used for a qualitative electron-microscopic investigation of the development of ciliated/microvillous surfaces of the olfactory epithelium.
Abstract: Rat foetuses from intra-uterine days E13 through E22 (day before parturition) and adults were used for a qualitative electron-microscopic investigation of the development of ciliated/microvillous surfaces of the olfactory epithelium. In the E13 and most of the E14 embryos the epithelial surface is not yet characteristically olfactory. Apical cell profiles show primary cilia. These can arise at the epithelial surface or below. From E14 onwards the epithelial surface acquires olfactory characteristics. Dendritic endings of the olfactory receptor cells can be found amidst microvillous profiles of supporting cells. Either cell type may bear primary cilia. From E16 onwards the receptor cells sprout multiple olfactory cilia, but cells with primary cilia are found throughout pre-natal development. These primary cilia are, at least for a while, retained during the formation of the secondary cilia. Primary cilia always have distinct necklaces at their base. Otherwise, especially with respect to their tips, their morphology can vary. Originally they have expanded tips (up to E14); later on such wide tips are no longer encountered (E16 and E17). Primary cilia of receptor cells never have wide tips. Appreciable numbers of endings with tapering olfactory cilia are discerned around E18 and especially E19. Throughout pre-natal development posterior/superior parts of the septal olfactory epithelium are more precocious than anterior/inferior parts, in particular in the region of transition with the respiratory epithelium. This advance in development includes total densities of dendritic endings of olfactory receptor cells, densities of multiciliated endings alone and lengths of supporting cell microvilli. This difference is discussed with respect to the topography of the olfactory epithelial surface in adult animals. In addition to the systematic topographic variation, a number of more local, apparently not-systematically distributed, topographic variations present during development are described. Most of these also occur in adult animals and they include heterogeneity in length of supporting cell microvilli and the presence of patches of supporting cells with rounded apical protuberances, of patches displaying dendrites with polyaxonemes rather than individual cilia and of scattered atypical cells (neither typical olfactory receptor nor olfactory supporting cells). At their surfaces such atypical cells can resemble inner-ear hair cells. Relative to olfactory receptor and supporting cells there are only very few atypical cells.(ABSTRACT TRUNCATED AT 400 WORDS)

89 citations

Journal ArticleDOI
TL;DR: The hypothesis that distal airways represent an important site for detecting changes in chronic obstructive pulmonary disease is supported, as an increased galectin-3 expression and neutrophil accumulation in the small airway epithelium was demonstrated, correlating with epithelial proliferation and airway obstruction.
Abstract: Galectins-1 and -3 regulate epithelial proliferation/apoptosis and neutrophil activation, and are implicated in lung cancer and asthma. The role of galectins in chronic obstructive pulmonary disease (COPD), characterised by epithelial changes and neutrophil infiltration, remains unknown. In the present study, galectin-1 and -3 expression was assessed by immunohistology in the bronchial epithelium of lung specimens from eight severe COPD patients and compared with nine nonsmokers and six smokers without COPD. Findings were related to epithelial proliferation (Ki-67), tissue inflammation and lung function. Epithelial galectin-3 immunostaining was increased only in the small airways of COPD patients when compared with nonsmokers and smokers. In contrast, galectin-1 was only significantly increased in the small airways of the group of smokers. Ki-67+ epithelial cells and neutrophils were increased in the small airways of COPD patients when compared with smokers. Furthermore, intra-epithelial neutrophils correlated in the small airways with Ki-67+ epithelial cells and with the forced expiratory volume in one second/forced vital capacity ratio. However, no correlation was observed with galectin expression. The present study supports the hypothesis that distal airways represent an important site for detecting changes in chronic obstructive pulmonary disease. In patients with severe disease, an increased galectin-3 expression and neutrophil accumulation in the small airway epithelium was demonstrated, correlating with epithelial proliferation and airway obstruction.

89 citations

Journal ArticleDOI
TL;DR: It is suggested that early BC-specific smoking-induced molecular changes are critical to the pathogenesis of COPD, and these represent a candidate target for novel therapeutic approaches to prevent COPD progression in susceptible individuals.
Abstract: The airway epithelium is the primary site of the earliest pathologic changes induced by smoking, contributing to the development of chronic obstructive pulmonary disease (COPD). The normal human airway epithelium is composed of several major cell types, including differentiated ciliated and secretory cells, intermediate undifferentiated cells, and basal cells (BC). BC contain the stem/progenitor cell population responsible for maintenance of the normally differentiated airway epithelium. Although inflammatory and immune processes play a significant role in the pathogenesis of COPD, the earliest lesions include hyperplasia of the BC population, suggesting that the disease may start with this cell type. Apart from BC hyperplasia, smoking induces a number of COPD-relevant airway epithelial remodeling phenotypes that are likely initiated in the BC population, including mucous cell hyperplasia, squamous cell metaplasia, epithelial–mesenchymal transition, altered ciliated and nonmucous secretory cell differentiation, and suppression of junctional barrier integrity. Significant progress has been recently made in understanding the biology of human airway BC, including gene expression features, stem/progenitor, and other functions, including interaction with other airway cell types. Accumulating evidence suggests that human airway BC function as both sensors and cellular sources of various cytokines and growth factors relevant to smoking-associated airway injury, as well as the origin of various molecular and histological phenotypes relevant to the pathogenesis of COPD. In the context of these considerations, we suggest that early BC-specific smoking-induced molecular changes are critical to the pathogenesis of COPD, and these represent a candidate target for novel therapeutic approaches to prevent COPD progression in susceptible individuals.

89 citations


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