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.

Human eosinophil major basic protein causes hyperreactivity of respiratory smooth muscle: role of the epithelium

Abstract: Major basic protein (MBP), one of several cationic proteins associated with the eosinophil granule, is cytotoxic to respiratory epithelium and is present in the sputum of asthmatics and on damaged bronchial epithelium from patients dying of asthma. The present experiments were performed in order to determine the effects of MBP on the responsiveness of airway smooth muscle. Rings of guinea pig trachea, in some of which the epithelium had been gently removed by rubbing, were incubated for 5 h in modified Krebs-Ringer bicarbonate solution containing buffer or human MBP (100 micrograms/ml). The tracheal rings were then suspended for isometric tension recording in organ chambers filled with Krebs-Ringer solution containing indomethacin. MBP did not affect the reactivity of rings in which the epithelium had been removed, but significantly augmented that of unrubbed rings to acetylcholine and histamine. The results suggest that MBP, by inhibiting the function of epithelial but not smooth muscle cells, causes hyperreactivity of respiratory smooth muscle, which may contribute to the hyperreactivity observed in chronic respiratory disease.

Mechanisms of Acid and Base Secretion by the Airway Epithelium

Abstract: One of the main functions of the airway epithelium is to inactivate and remove infectious particles from inhaled air and thereby prevent infection of the distal lung This function is achieved by mucociliary and cough clearance and by antimicrobial factors present in the airway surface liquid (ASL) There are indications that airway defenses are affected by the pH of the ASL and historically, acidification of the airway surfaces has been suggested as a measure of airway disease However, even in health, the ASL is slightly acidic, and this acidity might be part of normal airway defense Only recently research has focused on the mechanisms responsible for acid and base secretion into the ASL Advances resulted from research into the airway disease associated with cystic fibrosis (CF) after it was found that the CFTR Cl(-) channel conducts HCO (3) (-) and, therefore, may contribute to ASL pH However, the acidity of the ASL indicated parallel mechanisms for H(+) secretion Recent investigations identified several H(+) transporters in the apical membrane of the airway epithelium These include H(+) channels and ATP-driven H(+) pumps, including a non-gastric isoform of the H(+)-K(+) ATPase and a vacuolar-type H(+) ATPase Current knowledge of acid and base transporters and their potential roles in airway mucosal pH regulation is reviewed here

Intrinsic biochemical and functional differences in bronchial epithelial cells of children with asthma.

Abstract: Rationale: Convincing evidence of epithelial damage and aberrant repair exists in adult asthmatic airways, even in the absence of inflammation. However, comparable studies in children have been limited by access and availability of clinical samples.Objectives: To determine whether bronchial epithelial cells from children with asthma are inherently distinct from those obtained from children without asthma.Methods: Epithelial cells were obtained by nonbronchoscopic bronchial brushing of children with mild asthma (n = 7), atopic children without asthma (n = 9), and healthy children (n = 12). Cells were subject to morphologic, biochemical, molecular, and functional assessment. Responses were also compared with commercially available epithelial cultures and the transformed cell line 16HBE140.Results: All epithelial cells exhibited a “cobblestone” morphology, which was maintained throughout culture and repeated passage. Expression of cytokeratin 19 varied, with disease phenotype being greatest in healthy nonato...

Expression of the SARS-CoV-2 ACE2 Receptor in the Human Airway Epithelium.

Abstract: Rationale: Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease (COVID-19), a predominantly respiratory illness. The first step in SARS-CoV-2 infection is binding of the virus to ACE2 (angiotensin-converting enzyme 2) on the airway epithelium.Objectives: The objective was to gain insight into the expression of ACE2 in the human airway epithelium.Methods: Airway epithelia sampled by fiberoptic bronchoscopy of trachea, large airway epithelia (LAE), and small airway epithelia (SAE) of nonsmokers and smokers were analyzed for expression of ACE2 and other coronavirus infection-related genes using microarray, RNA sequencing, and 10x single-cell transcriptome analysis, with associated examination of ACE2-related microRNA.Measurements and Main Results: 1) ACE2 is expressed similarly in the trachea and LAE, with lower expression in the SAE; 2) in the SAE, ACE2 is expressed in basal, intermediate, club, mucus, and ciliated cells; 3) ACE2 is upregulated in the SAE by smoking, significantly in men; 4) levels of miR-1246 expression could play a role in ACE2 upregulation in the SAE of smokers; and 5) ACE2 is expressed in airway epithelium differentiated in vitro on air-liquid interface cultures from primary airway basal stem/progenitor cells; this can be replicated using LAE and SAE immortalized basal cell lines derived from healthy nonsmokers.Conclusions: ACE2, the gene encoding the receptor for SARS-CoV-2, is expressed in the human airway epithelium, with variations in expression relevant to the biology of initial steps in SARS-CoV-2 infection.