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The patient with acute respiratory problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
It was once thought that the respiratory epithelial cells simply acted as a barrier to protect the inner layers of the respiratory tree. The respiratory epithelium does indeed have a huge role to play in protection. For most sections of the respiratory tree, each epithelial cell has around 200 tiny hair-like projections called cilia. On top of the cilia sits a blanket of mucus, which is constantly moved upwards by the cilia, all beating in the same direction (1000 beats per minute). Any debris in the air is thus trapped and moved upwards by the muco-ciliary escalator to be expectorated or swallowed. The creation of mucus (up to 100mL each day) is extremely complex, but contributing are goblet cells, which secrete mucus, as well as submucosal glands found throughout the respiratory tract. Pathology, smoking, dehydration and dry gases (including O2 therapy) can decrease the effectiveness of this protective mechanism. Additional defences include Immunoglobulin A (IgA), an antibody produced by B lymphocytes and secreted onto the respiratory surface, irritant receptors and the cough reflex, as well as lymphoid tissue and phagocytic macrophage cells in the alveolar wall.
Epithelial Cells
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
The respiratory epithelium is classically viewed as a simple interface between the host and its environment. In fact, it is a remarkably developed tissue comprising a variety of cell types with specialized functions. Adhesion molecules are expressed on the surface of epithelial cells and are crucial to their interactions with the surrounding microenvironment. Moreover, epithelial cells play an active role in the inflammatory response by secreting an array of mediators, including cytokines, lipid and peptide products, and reactive oxygen species. The broad range of phenotypes, surface marker expression, and mediators secreted by the epithelium of the lung will be discussed in this chapter.
Bronchus-associated lymphoid tissue and immune-mediated respiratory diseases
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Dale T. Umetsu, Bart Lambrecht
Although the respiratory epithelium has been traditionally thought to be primarily a physical barrier and a base for ciliary activity, it is now clear that respiratory epithelial epithelium has a major role in sensing the environment, maintaining homeostasis, and repairing injury. Airway epithelial cells respond to microbial challenge and environmental insults by rapidly producing an array of cytokines and growth factors that initiate innate immunity, prime adaptive immunity, and establish homeostasis. For example, airway epithelial cells respond to PAMPs associated with antigens or microbes that enter the airways, through toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD)-like receptors, and C-type lectin receptors. Signals generated by these receptors or due to direct injury of epithelial cells induce lung epithelial cells to produce cytokines such as interleukin (IL)-1, IL-25, IL-33, thymic stromal lymphopoietin (TSLP), granulocyte-macrophage colony-stimulating factor (GM-CSF), and transforming growth factor (TGF)-β, as well as chemokines (CCL20 [MIP-3α; ligand of CCR6], CCL17 [TARC; ligand of CCR4], and CCL22 [MDC; ligand of CCR4]) and antimicrobial peptides such as defensins. Epithelial cells are also a copious source of endogenous danger signals like adenosine triphosphate (ATP), uric acid, and high mobility group box 1 (HMGB1) that can alert immune cells. Thus, epithelial cells can initiate innate immunity that can later affect adaptive mucosal immunity.
Diagnostic and therapeutic approaches for elderly asthma patients: the importance of multidisciplinary and multidimensional management
Published in Expert Review of Respiratory Medicine, 2023
Alida Benfante, Alessandra Tomasello, Enrico Gianquinto, Maria Noemi Cicero, Nicola Scichilone
A condition of reduced elastic recoil could reasonably account for the attenuation of deep-inspiration-induced bronchodilation, due to a diminished stretching the airways [27,28]. Moreover, inflammatory processes of the airways enhanced by aging could be involved in the development of increasing nonspecific airway responsiveness with aging [29,30]. Neuronal mechanisms are implicated in the regulation of the activity of bronchial smooth muscle and with advanced age, changes occur that result into increase in the smooth muscle contractility. This is a consequence of the impact of mediators that are released by the damaged respiratory epithelium after long-term exposure to smoking or pollution. Another important factor cited in literature is the imbalance between adrenergic and cholinergic fibers, which leads to increased bronchial muscle tone. In terms of methacholine-induced changes in FVC, the airways of elderly patients with asthma are more reactive than those of young patients. It has been documented an exaggerated airway closure in the elderly asthmatics leading to a significant reduction in FVC, rather than in FEV1, during a broncho-provocation challenge. This denotes that elderly asthmatic patients are at higher risk of airway closure and dramatic episodes of bronchospasms [29].
Amorphous silica nanoparticles caused lung injury through the induction of epithelial apoptosis via ROS/Ca2+/DRP1-mediated mitochondrial fission signaling
Published in Nanotoxicology, 2022
Yan Li, Yawen Zhu, Bosen Zhao, Qing Yao, Hailin Xu, Songqing Lv, Ji Wang, Zhiwei Sun, Yanbo Li, Caixia Guo
Based on these issues, we investigated the pulmonary impairments and related mechanisms caused by SiNPs using in vivo and in vitro models. A preliminary pulmonary injury was evaluated by establishing a subacute SiNPs exposure model in Wistar rats via intratracheal instillation. The respiratory epithelium serves a critical role for the maintenance of airway integrity and defense against inhaled particles, and also as a source of various cytokines, chemokines (Gohy et al. 2016). In vitro, human bronchial epithelial cell (16HBE) was applied, a reliable in vitro model to assess the inhalational toxicity of NPs. Different endpoints were determined, including intracellular ROS level, mitochondrial structure and function, mitochondrial dynamics, and apoptosis. More importantly, the mode of action, cross-interaction, and signaling cascades were determined by using inhibitors.
The effect of COVID-19 on nasal mucociliary clearance
Published in Acta Oto-Laryngologica, 2022
Ebru Ozer Ozturk, Mehmet Aslan, Tuba Bayındır
The respiratory epithelium has a critical role in infection protection. While the goblet cells in the respiratory epithelium release mucus, the ciliated cells that account for more than half of the epithelial cells move the overlying mucus layer towards the oropharynx [4]. Mucus protects the respiratory tract against harmful chemical, microbiological, and physical influences. Microorganisms are captured by the mucus layer in the respiratory system and kept away from the respiratory epithelial cell surface, and the ciliated cells remove them from the microenvironment. This innate defense system is called mucociliary clearance (MCC) [5]. Nasal mucus is transported to the oropharynx by efficient and coordinated nasociliary activity, adhering to inhaled particles or microorganisms [6]. Nasal MCC is the respiratory system's principal defense mechanism [7]. Impairment of nasociliary activity can cause acute or chronic infections of the upper and lower respiratory system.