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Epithelial Function and Airway Responsiveness
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
Roy G. Goldie, Janet M. H. Preuss
Cells in the airway epithelium secrete a diverse array of materials, including mucus, water, and electrolytes,149,150 as part of the complex of defence mechanisms to protect the lungs from harmful substances inhaled from the external environment. The epithelium presents the first barrier to allergens by providing a blanket of mucus over the airway surface which traps allergens for transport back to the pharynx by the beating cilia. The mucus contains proteolytic enzymes which also degrade allergens.151 In healthy airways, the production of mucus is limited to provide an adequate system for airway lubrication and the entrapment of inhaled foreign particles. However, the amount, composition, and viscosity of mucus may be altered in airway diseases, including viral infections, asthma, bronchitis, and cystic fibrosis.1,152,153 In the larger airways, submucosal glands provide the bulk of the material secreted to the airway surface.1,3,6 However, epithelial serous, goblet, and Clara cells also contribute significantly to airway mucus production.154,155
Epithelial Cells
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Serous cells are another class of secretory cells that contribute to the fluid bathing the surface of the epithelium. In contrast to goblet cells, however, they produce low-viscosity secretions rich in lysozyme, neutral glycoprotein, and the epithelial transfer component of IgA (16). Electron microscopy has demonstrated that the secretory granules of serous cells are electron-dense, whereas those of goblet cells are electron-lucent (1). Serous and mucus cells are also the two cell types that line the submucosal glands that are found throughout the larger airways.
Respiratory System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Tom P. McKevitt, David J. Lewis
Mucosal necrosis is characterized by cytoplasmic eosinophilia, nuclear pyknosis/karryohexis, and cellular exfoliation. Necrosis triggers an inflammatory response, and continued exfoliation will result in erosion or ulceration of the mucosa. Repair can begin once the toxic insult is removed, but the outcome depends on the severity of the insult. All epithelium types lining the nasal cavity are capable of full repair; however, metaplasia or postnecrotic atrophy may be seen following chronic or severe injury. Regenerating surface epithelium may seal the excretory ducts of submucosal glands, blocking their outflow and leading to pressure atrophy and ectasia, with hypertrophy of adjacent unaffected glands. Atrophy of the nerve bundles within the lamina propria often occurs following necrosis of olfactory epithelium. Another possible sequel to epithelial necrosis is turbinate fusion, resulting mainly from organization of the associated inflammatory exudate or from contact between denuded areas of basement membrane. Severe necrosis can extend through the submucosa to affect the underlying submucosal glands directly and the nasal septum/bone. Epithelial necrosis and suppurative inflammation were seen in the nasal cavity of rats following a 1-month inhalation study with the β-agonist tulbuterol hydrochloride (Dudley et al. 1989).
Current status and advances in esophageal drug delivery technology: influence of physiological, pathophysiological and pharmaceutical factors
Published in Drug Delivery, 2023
Ai Wei Lim, Nicholas J. Talley, Marjorie M. Walker, Gert Storm, Susan Hua
The esophageal mucus is thought to act as a buffer layer on the surface of the mucosa to neutralize and protect the esophagus from stomach refluxates. It also plays a role in the innate immune system that forms a barrier against pathogens (Sarosiek & McCallum, 2000; Nochi & Kiyono, 2006). Mucus is produced in the esophagus mainly by the esophageal submucosal glands. These glands are connected to the lumen of the esophagus via small ducts that are located between the submucosa and mucosa of the epithelium (Meyer et al., 1986). Esophageal mucus contains a mixture of mucin, proteins (e.g. threonine 16.3%, serine 14.2%, glycine 8.9%, glutamine 8.5%, alanine 8.4%, proline 8.0%, asparagine 7.6%, leucine 6.9%, valine 5.7%, lysine 3.3%, isoleucine 2.8%, histidine 2.6%, arginine 2.6%, phenylalanine 2.6%, and tyrosine 1.1% (Namiot et al., 1994)), polypeptides (e.g. epidermal growth factors, prostaglandin E2, and immunoglobulin A (Sarosiek et al., 1993, 1994)), phospholipids, and bicarbonate ions (Namiot et al., 1994).
Effect of Hesperidin against Induced Colon Cancer in Rats: Impact of Smad4 and Activin A Signaling Pathway
Published in Nutrition and Cancer, 2022
Sahar E. M. El-Deek, Sary K. H. Abd-Elghaffar, Randa S. Hna, Heba G. Mohamed, Heba E. M. El-Deek
Control group rats exhibited normal mucosal and submucosal layers with no signs of abnormalities. Hsd-treated rats also showed normal histological structure with increased numbers of goblet cells. DMH induction caused severe deterioration within colonic tumors in exposed rats. DMH-treated rats showed adenomatous polyps with severe dysplasia. Dysplasia was characterized by enlarged, hyperchromatic and elongated nuclei arranged in a stratified configuration along the basement membrane. Dysplastic glandular tissue exhibited a serrated appearance and thickening of the epithelium. Supplementation with Hsd throughout the experiment resulted in adenomas with mild dysplastic changes compared with the DMH group. There was evidence of necrosis of some glandular tissue and lymphocytic infiltration in between glands. Colon sections of the DMH followed by Hsd administration group showed few changes compared with the DMH group. There were severe dysplastic changes in the submucosal glands. Scattered lymphocytic infiltration between hyperplastic glands was also present (Figure 3).
Therapeutic effect of statins on airway remodeling during asthma
Published in Expert Review of Respiratory Medicine, 2022
Mashael Alabed, Noha Mousaad Elemam, Rakhee K Ramakrishnan, Narjes Saheb Sharif-Askari, Tarek Kashour, Qutayba Hamid, Rabih Halwani
Several structural alterations start early in asthma and are observed even in children [11–13]. In asthma, the epithelial changes due to airway remodeling include epithelial shedding, goblet cell hyperplasia, loss of ciliated cells, upregulation of growth factor release such as TGF-β1, epidermal growth factor receptor (EGFR) ligands, and the overexpression of receptors such as EGFR. The loss of airway surface epithelium and the resultant denudation of the basement membrane impairs this protective physical barrier, increasing the predisposition of asthmatic airways to allergic insult [14–18]. Clinically, the degree of epithelial loss is correlated with the degree of hyperresponsiveness in asthmatic subjects [19], indicating that the degree of epithelial turnover is thus related to the development of asthma and its severity. In addition, asthmatic patients also exhibit goblet cell hyperplasia and submucosal gland hyperplasia [20], which lead to excessive mucus secretion, and consequent narrowing of the airways, and increased airway wall thickness [14].