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Application of Stem Cell and Exosome-Based Therapy in COVID-19
Published in Debmalya Barh, Kenneth Lundstrom, COVID-19, 2022
Suleyman Gokhan Kara, Ayla Eker Sariboyaci
MSCs are being tested in lung damage caused by COVID-19 through their ability of endothelial and epithelial repair, bacterial and alveolar fluid clearance, and their anti-inflammatory and anti-apoptotic effects. COVID-19 pneumonia occurs because of damage to the alveoli. It is necessary to know alveolar histopathology to understand the mechanism of damage. The alveolar epithelium consists of Type I and Type II pneumocytes. Type I pneumocytes occupy 95% of the alveolar surface and are responsible for gas exchange, while Type II pneumocytes secrete surfactant, reduce alveolar surface tension, and protect from alveolar collapse. In COVID-19 pneumonia, Type II pneumocytes become infected by the virus, and cell death occurs. The decrease in surfactant causes alveolar collapse. The migration of inflammatory cells and mediators into the alveoli results in the development of alveolar oedema. As a result of these events, cell death also occurs in Type I pneumocytes. Lung alveolar epithelium has limited regeneration. Type I pneumocytes are unable to replicate. In the event of damage, Type II pneumocytes can proliferate and differentiate into Type I pneumocytes. The function of this repair mechanism changes according to the extent of the damage. When alveolar damage is mild, a repair mechanism preserves lung function. However, if there is extensive alveolar damage, fibrosis or emphysema develops, and the alveoli lose their function.
Epithelial Cells
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
The epithelial cells of the alveoli are designated alveolar type I and type II cells. Type I cells cover almost 95% of the alveolar surface and have a flattened morphology that allows for efficient gas exchange (3). In contrast, alveolar type II cells are cuboidal and occur at the junction of alveolar septae (5). Although they constitute only about 5% of the alveolar surface, type II cells represent 60% of alveolar cells by number (40). Their exposed surface is covered with microvilli, and their cytoplasm contains characteristic lamellated inclusion bodies. Phospholipids and proteins are found in these organelles and are released to form the surfactant of the lung (41,42). Type II cells also produce several proteins of the classical and alternative complement pathways (43). The type II cell is the stem cell of the alveolar epithelium. When the alveolar surface is damaged by exposure to oxidants or other injurious agents, the type II cells rapidly divide, repopulate the area, and then differentiate into type I cells (44).
Acute Alveolar Injury: Experimental Models
Published in Joan Gil, Models of Lung Disease, 2020
The above evidence, taken together, provides strong support for the hypothesis that complement-activated neutrophils can cause injury to pulmonary endothelium. The relationship of this type of injury to acute alveolar injury in the human is less clear. The severity of the experimental process does not approach that of the human lesion and injury to alveolar epithelium has not been described. Species differences, the very short duration of the experiments reported to date, or factors which intensify the acute inflammatory response in the human condition may, singly or in some combination, explain the morphologic differences. Nevertheless, until the histologic picture of human AAI is more closely reproduced, conclusions about the role of complement activation and neutrophil sequestration in human AAI must be tentative.
Adverse pulmonary effects after oral exposure to copper, manganese and mercury, alone and in mixtures, in a Spraque-Dawley rat model
Published in Ultrastructural Pathology, 2023
M Draper, Mj Bester, M Van Rooy, Hm Oberholzer
Air pollutants can cause severe lung injury and pathology, such as asthma and COPD. Bronchiole epithelium is the first line of defense against air particulate and pollutants. In the lungs the alveolar wall separates adjacent alveoli, which arise from the respiratory bronchioles.36,37 The alveolar wall consists of the lining alveolar epithelium, interstitium and the capillary of the endothelium forming the air-blood barrier for gaseous exchange.37 The alveoli are stabilized and protected from over-distension and collapse by connective tissue and a surfactant layer, secreted by the type II pneumocytes. The inter-alveolar wall must provide stability, flexibility, and a large thin surface area for the effective diffusion of oxygen and carbon dioxide.38Although the effects of air pollution and associated heavy metals on the respiratory system are known, there is a lack of studies on the effect of orally exposed heavy metals on the respiratory system.
Assessment of vaping devices as an alternative respiratory drug delivery system
Published in Drug Development and Industrial Pharmacy, 2022
Zaid Khaled, Eman Zmaily Dahmash, Jasdip Koner, Raad Al Ani, Hamad Alyami, Abdallah Y. Naser
The respiratory tract has generated significant interest as an alternative drug delivery route, with advantages including reduced systemic side effects, the ability to deliver higher doses of the active pharmaceutical ingredient (API) to the local site of action, and a patient friendly route of delivery. An additional key advantage of pulmonary delivery is that the lungs offer a route into the bloodstream that bypasses first-pass metabolism, while offering a large absorptive surface area (∼100 m2), a very thin absorption membrane (0.1–0.2 μm), and elevated blood flow (5 l/min), which facilitate uptake and distribution of the APT throughout the body. The alveolar epithelium of the lung is an absorption site for several therapeutics and macromolecules, targeting local respiratory diseases such as asthma and chronic pulmonary infections or systemic delivery of drugs such as insulin, growth hormones, and oxytocin [1–5].
Is Claudin 4 a Player to Be Reckoned with or Not in the Context of Lung Transplantation?
Published in Journal of Investigative Surgery, 2022
Anna Niroomand, Sandra Lindstedt
PGD that may then follow the IRI is a form of acute lung injury in which edema occurs in both the airspaces and in alveoli. The removal of edema from the air spaces is a critical function of the alveolar barrier but requires intact tight junctions. The endothelial injury that occurs in ischemic injury prior to PGD exacerbates the formation of edema [7]. Alveolar fluid clearance has been associated with increased survival in patients with acute lung injury but has also been associated with pulmonary graft function after transplantation [8]. The alveolar epithelium is a heterogeneous monolayer of cells interconnected by tight junctions at sites of cell-cell contact. Paracellular permeability depends on claudin-family tight junction proteins. The claudin family consists of about 10 to 20 alveolar claudins that are expressed differently throughout the alveolar epithelium.