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Lung Mechanobiology
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Daniel J. Tschumperlin, Francis Boudreault, Fei Liu
The mechanical challenge in distributing gas and blood in suitable proportions is great: the lung's delicate structure must be compliant and elastic to allow lung inflation and deflation with minimal effort, yet stable to prevent collapse of the airway and alveoli. The stability of this arrangement depends crucially on pulmonary surfactant, a complex mixture of phospholipids and proteins synthesized by specialized cells within the epithelial lining of the alveoli.3 Pulmonary surfactant lowers surface tension in alveoli, and possesses the unique characteristic that it drives surface tension toward zero during dynamic film compression, helping to stabilize alveoli during lung deflation.4 Both acute and chronic derangements of the lung's delicate microstructure and surfactant system ultimately lead to inadequate gas exchange and, in extreme cases, to respiratory failure. Understanding the physical origin of lung mechanical function, and the mechanism of failure in various disease states, is central to the study of respiratory physiology and medicine. In this chapter, we focus on efforts to elucidate the cellular, molecular, and microstructural mechanisms underpinning mechanobiological function of the lung in health and disease.
Nasal and Pulmonary Drug Delivery Systems
Published in Ambikanandan Misra, Aliasgar Shahiwala, In-Vitro and In-Vivo Tools in Drug Delivery Research for Optimum Clinical Outcomes, 2018
Pranav Ponkshe, Ruchi Amit Thakkar, Tarul Mulay, Rohit Joshi, Ankit Javia, Jitendra Amrutiya, Mahavir Chougule
The lung consists of around 40 cell types. The alveolar epithelium, endothelium, and interstitial cell layer are present at the interface where the alveolar gas exchange primarily transpires. Pneumonocytes (alveolar epithelial cells, type I and type II) together form the analveolar wall. The gas exchange is the most important function of type I cells, while the production and secretion of lung surfactant is the function of type II cells. There is 0.5-μm distance between the air within the alveoli and capillaries, which leads to the gas exchange via diffusion due to a partial pressure gradient at the interface. Along with mucus that is coated onto the alveoli, phospholipids and surface protein form analveolar fluid. Pulmonary surfactants lower the surface tension and are vital for operating the proper gas exchange. Pulmonary surfactants are a mixture of 90% lipids and 10% protein secreted by type II alveolar cells, whose primary role is to decrease the surface tension formed at the air/liquid interface within the alveoli of the lung. The additional functions of these surfactants include elevating the pulmonary compliance, facilitating and recruiting collapsed airways, and preventing the collapse of the lung at the end of expiration. The surfactants present in lungs are dipalmitoylphosphatidylcholine (DPPC), phosphatidylglycerol (PG), lysophosphatidic acid (PA), phosphatidylethanolamine (PE), phosphatidylinositol (PI), and cholesterol. Apart from surfactants, two groups of proteins are present in pulmonary surfactants. Surfactant proteins A, B, C, and D are the designated proteins, of which surfactant protein B and surfactant protein C are small hydrophobic proteins, while surfactant protein A and surfactant protein D are large hydrophilic proteins (Patton 1996).
Biosurfactants
Published in Girma Biresaw, K.L. Mittal, Surfactants in Tribology, 2019
Dina A. Ismail, Mona A. Youssif, Nabel A. Negm
The use of surfactants as agents for stimulating stem fibroblast metabolism and immunomodulatory action has been reported. However, it has also been reported that the deficiency of a pulmonary surfactant, a phospholipid protein complex, is responsible for the failure of respiration in premature infants. However, isolation of its genes from its protein molecules and cloning it in bacteria has made possible its medical application through production by fermentation [109].
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
The defense mechanisms of the airways and lung comprise the cough reflex, the epithelial barrier and lining fluid, the mucociliary escalator, metabolic signaling cascades (e.g., activation of cytochrome P450 family and and/or activation of nuclear factor erythroid 2–related factor 2 (Nrf2)-mediated transcription factors), humoral factors including antimicrobial and surfactant peptides or complement proteins and cells that elicit immune responses, namely epithelial cells, macrophages, monocytes, dendritic cells, neutrophils, natural killer cells, and mast cells (Hastedt et al. 2016; Rothen-Rutishauser et al. 2008). In the large airways, the epithelial lining fluid is composed of a superficial mucus layer overlying a periciliary liquid layer that is responsible for mucociliary clearance through physical unidirectional cilia movement and removal of deposited particles and gases dissolved in the mucus from the respiratory tract (Schuster et al. 2013). Further, the alveolar surface is covered by pulmonary surfactant that also plays a critical role in the clearance of inhaled toxicants including aerosolized (nano)particles (Wohlleben et al. 2016).