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Biology of Coronaviruses with Special Reference to SARS-CoV-2
Published in Joystu Dutta, Srijan Goswami, Abhijit Mitra, COVID-19 and Emerging Environmental Trends, 2020
Joystu Dutta, Srijan Goswami, Abhijit Mitra
The damaged Type-II pneumocytes release specific inflammatory mediators, which are responsible for triggering and stimulating the macrophages. Stimulated macrophages secrete specific cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). These cytokines reach the bloodstream and cause the endothelial cells to undergo dilation. This cytokine action causes smooth muscle to dilate and increase the capillary permeability by contraction of endothelial cells. Consequently, the plasma starts flowing out and leaking into interstitial space and potentially into alveoli. Accumulation of fluid results in the compression of alveoli. Some of the fluid may try to enter into alveoli, and if a certain concentration of fluid enters alveoli, it leads to a condition called alveolar edema. Alveolar edema leads to the drowning out of the surfactants, which results in increased surface tension. As the surface tension increases, the collapsing pressure also increases, and as a result, the alveoli collapse, which is termed as alveolar collapse. The accumulation of a significant amount of fluid around the alveoli impairs the alveolar membrane (respiratory membrane), which results in decreased gas exchange. Decreased gas exchange leads to hypoxemia, which can be indicated as increased work of breathing (acute respiratory distress syndrome) (Open WHO, 2020; Lim et al., 2016; Shang et al., 2020; Yuki et al., 2020; Mason, 2020; Fehr et al., 2015; Abbas et al., 2004).
Organoid Technology for Basic Science and Biomedical Research
Published in Hyun Jung Kim, Biomimetic Microengineering, 2020
Szu-Hsien (Sam) Wu, Jihoon Kim, Bon-Kyoung Koo
Another type of murine lung organoid has been generated from a different region of the airway, the alveoli. Alveoli are the place where the actual gas-exchange takes place and consist of two types of cells: alveolar type 1 and 2 (AT1 and AT2, respectively). Desai, Brownfield, and Krasnow (2014) demonstrated both AT1 and AT2 derive from the same progenitors, but the rare population of AT2 cells also function as stem cells to provide AT1 cells for alveolar renewal. The authors showed that the EGFR pathway regulates the stem cell potential of AT2 cells in vitro and that oncogenic KRAS causes dysregulation in vivo. In addition to these studies, Lee et al. (2014) have recently established a co-culture system of bronchioalveolar stem cell-derived lung organoids and endothelial cells and have used the system to demonstrate the multipotency of bronchioalveolar stem cells and their differentiation into both bronchiolar and alveolar cells in vitro.
Computer-Aided Diagnosis of Chronic Obstructive Pulmonary Disease Using Accurate Lung Air Volume Estimation in Computed Tomographic Imaging
Published in Ayman El-Baz, Jasjit S. Suri, Lung Imaging and CADx, 2019
Hadi Moghadas-Dastjerdi, Mohammad Reza Ahmadzadeh, Abbas Samani
According to World Health Organization reports, lung diseases are among the leading causes of death around the world. The death rate due to lung diseases is still on the rise, while other causes of death, such as cancer and stroke, are declining. Among all pulmonary disorders, chronic obstructive pulmonary disease (COPD) is one of the most prevalent and fatal diseases. About 7% of the global population is affected by this disease, leading to an economic burden estimated at $2.1 trillion in 2010 [1]. The main effect of COPD is the lung's air ventilation reduction, which may occur due to two different mechanisms. The first mechanism is the obstruction of small airways as a result of clogging by mucus or as a consequence of shape change. The second mechanism, emphysema, involves destruction of the alveoli's wall and a reduction of the elasticity of the alveoli sacs and consequently a reduction of the gas–blood exchange surface. In general, these two mechanisms lead to the limitation of airflow throughout respiration and immobility of old inhaled air in the lungs, referred to as air trapping. The trapped air has no beneficial function in the pulmonary system, as it includes a low amount of oxygen and a high amount of carbon dioxide.
Compositional variations in metal nanoparticle components of welding fumes impact lung epithelial cell toxicity
Published in Journal of Toxicology and Environmental Health, Part A, 2023
Li Xia, Jae Hong Park, Katelyn Biggs, Chang Geun Lee, Li Liao, Jonathan H. Shannahan
The predominant cell type within the lung is epithelial cells. These serve important functions such as barrier protection, fluid balance, clearance of particulates, initiation of immune responses, mucus and surfactant production, and coordination of repair after injury. The alveolar epithelium includes alveolar type I and alveolar type II cells. Type I cells comprise the alveolar epithelium and facilitate gas exchange within the lung. Type II cells secrete surfactant proteins which are critical to stabilize the structure of alveoli. Human alveolar type II A549 cells have been extensively utilized as an in vitro model to examine the pulmonary epithelium’s response to exposures including particulates and are particularly useful in studying pulmonary metabolic processes. In our current study, A549 cells were used for the initial examination of the cellular consequences associated with compositional variations in metal NP components.
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
Patients diagnosed with emphysema exhibit mucous cell hyperplasia, resembling manifestations of chronic bronchitis. These individuals exhibit destruction of lung parenchymal tissues and alveolar septal walls, which result in airspace enlargement. Destruction of alveolar walls includes loss of the alveolar capillary bed and alveolar surface area, which impairs gas exchange. One potential mechanism underlying alveolar loss involves proteases released by the sustained recruitment, retention, and activation of inflammatory cells, or by alveolar and bronchial epithelial cells following exposure to toxic irritants, allergens, or TS (Churg, Zhou, and Wright 2012; Fischer, Voynow, and Ghio 2015). Loss of alveolar septa reduces lung function, increases compliance (reduces elastance), and induces breathlessness and hyperventilation (Boutou et al. 2015; Suki et al. 2013). In smokers, the loss contributes to persistent airway inflammation (Barnes 2016b; Gamble et al. 2007) and airflow obstruction. Host genetic predisposition also induces COPD pathogenesis and symptoms (Alam et al. 2014; Silverman 2020; Sorroche et al. 2015).
Assessing the in vitro toxicity of airborne (nano)particles to the human respiratory system: from basic to advanced models
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Maria João Bessa, Fátima Brandão, Fernanda Rosário, Luciana Moreira, Ana Teresa Reis, Vanessa Valdiglesias, Blanca Laffon, Sónia Fraga, João Paulo Teixeira
Another important aspect to take into consideration is how physiological fluids might change the physicochemical properties and behavior of (nano)particles (Urban et al. 2016). Upon contact with the biological pulmonary milieu, (nano)particles may become surrounded by biomolecules such as albumin and proteins in the surfactant, which significantly contribute to the formation of a corona around them and change particle size and kinetics in the airways (Monopoli et al. 2012). In the alveolar region, (nano)particles interact with the lipids present in the surfactant film located at the air-liquid interface (ALI) in the epithelial lining fluid covering the internal surface of the lung (Raesch et al. 2015). The surfactant helps to stabilize the alveoli and promotes clearance of inhaled particles to maintain alveoli in a sterile- and inflammation-free environment (Kendall and Holgate 2012). Accordingly, characterization of nano-sized materials in relevant pulmonary biological fluids is of utmost importance (Wohlleben et al. 2016).