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.

Ciliostasis and loss of cilia induced by Mycoplasma hyopneumoniae in porcine tracheal organ cultures.

Abstract: In vivo- and in vitro-grown Mycoplasma hyopneumoniae organisms were inoculated onto newborn piglet tracheal organ cultures to provide a model for interaction of this organism with ciliated respiratory epithelium. Ciliostasis and loss of cilia in tracheal rings were induced by M. hyopneumoniae grown in vivo and with low-passage cultures when grown in vitro. Levels of calmodulin or dehydrogenase enzymes in tracheal ring epithelium were not altered even though ciliostasis and loss of cilia induced by M. hyopneumoniae were extensive. The capacity for inducing epithelial damage diminished with in vitro passage of the organism. Attempts to induce higher-passage cultures to attach to cilia, cause ciliostasis, or cause ciliary damage by supplementation of mycoplasmal medium with porcine lung extract failed. Epithelial damage induced by M. hyopneumoniae in tracheal rings was averted by using porcine immune serum or by separating the organisms from ciliated epithelium with a 0.1-microns-pore-size membrane. Attachment, or at least close association, of M. hyopneumoniae to ciliated epithelium appeared to be necessary to induce ciliostasis and loss of cilia in this model.

Biochemical transformation of regenerating ocular surface epithelium.

Abstract: Several biochemical parameters, including glycogen levels, and the activities of hexokinase, phosphorylase, and lactate dehydrogenase have been compared in regenerating epithelium of conjunctival and corneal origin in rabbits. The study was designed to determine the extent of biochemical transformation of conjunctival into corneal epithelium completed within 6 weeks. Although histological transformation, especially in the case of the chemically damaged eyes, is not. Glycogen and lactate dehydrogenase levels remained well below normal corneal epithelial levels for the period of observation.

Analysis of ACE2 in polarized epithelial cells: surface expression and function as receptor for severe acute respiratory syndrome-associated coronavirus.

Abstract: The primary target of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is epithelial cells in the respiratory and intestinal tract. The cellular receptor for SARS-CoV, angiotensin-converting enzyme 2 (ACE2), has been shown to be localized on the apical plasma membrane of polarized respiratory epithelial cells and to mediate infection from the apical side of these cells. Here, these results were confirmed and extended by including a colon carcinoma cell line (Caco-2), a lung carcinoma cell line (Calu-3) and Vero E6 cells in our analysis. All three cell types expressed human ACE2 on the apical membrane domain and were infected via this route, as determined with vesicular stomatitis virus pseudotypes containing the S protein of SARS-CoV. In a histological analysis of the respiratory tract, ACE2 was detected in the trachea, main bronchus and alveoli, and occasionally also in the small bronchi. These data will help us to understand the pathogenesis of SARS-CoV infection.

Proliferation and differentiation in mammalian airway epithelium.

Abstract: The infrequency of mitotic figures led to dispute amongst early workers as to the occurrence of cell division in adult mammalian airway epithelium [30, 63, 83, 227]. It was not until 1951 that quantitative work in the respiratory tract began to concentrate on the distal (i.e. respiratory) portion of the lung (reviewed by BERTALANFFY (20, 21], KAUFFMAN [132], and MASSE et al. [159]). Studies of the lining epithelium of conducting airways soon followed [I I, 25, 26, 27, 32, 38, 148, 208, 230]. The present review summarizes the results of many studies of cell division and differentiation in conducting airway epithelium. I t is divided into three major sections: I) general principles and techniques used in assessment of cell kinetics; 2) normal proliferation and differentiation in conducting airways and 3) effects of irritants and carcinogens, mechanical trauma, drugs, infection and physiological factors on cell proliferation and differentiation. Proliferation and differentiation, which occur during airway development, are not discussed here: the interested reader is referred to the following papers and reviews [24, 47, 119, 129, 132, 207, 237]. At least eight epithelial cell types are recognised in the lining epithelium of conducting airways and three in the epithelium lining the alveoli (for reviews see [41, 116, 117, 118]). In man the tracheobronchial surface epithelium is pseudostratified, ciliated and columnar

Remodeling in response to infection and injury. Airway inflammation and hypersecretion of mucus in smoking subjects with chronic obstructive pulmonary disease.

Abstract: Airway epithelium represents the first line of defense against toxic inhalants. In some subjects, cigarette smoking causes airway inflammation, hypersecretion of mucus, and poorly reversible airflow limitation through mechanisms that are still largely unknown. Likewise, it is unclear why only some smokers develop chronic obstructive pulmonary disease (COPD). Two cell types consistently result in relation to chronic airflow limitation in COPD: neutrophils and CD8(+) cells. Neutrophils are compartmentalized in the mucosal surface of the airways and air spaces, that is, the epithelium and lumen, whereas CD8(+) cells exhibit a more extensive distribution along the subepithelial zone of the airways and lung parenchyma, including alveolar walls and arteries. This pattern of inflammatory cell distribution is observed in mild or moderate COPD, and in patients who have developed COPD, it is not modified by smoking cessation. The number of neutrophils further increases in the submucosa of patients with severe COPD, suggesting a role for these cells in the progression of the disease. Hypersecretion of mucus is a major manifestation in COPD. Mucus is produced by bronchial glands and goblet cells lining the airway epithelium. Unlike mucous gland enlargement, greater mucosal inflammation is associated with sputum production. Whereas neutrophil infiltration of submucosal glands occurs only in smokers with COPD, goblet cell hyperplasia in peripheral airways occurs both in smokers with or without COPD, suggesting that the major determinant of goblet cell hyperplasia is cigarette smoke itself.