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Epidemiology and pathophysiology of exercise-induced bronchoconstriction in athletes
Published in John W. Dickinson, James H. Hull, Complete Guide to Respiratory Care in Athletes, 2020
Pascale Kippelen, Andrew Simpson
Bronchial biopsies and induced sputum are more direct approaches to demonstrate airway inflammation and injury. However the complexity and invasiveness of these techniques renders them difficult to use in athletes (hence, seldom experimental data based on bronchial biopsies and sputum analyses) and preclude them from being routinely implemented in clinical practice (Table 4.2). A non-invasive alternative is the measurement of the club cell secretory protein-16 (CC16) in urine or serum. CC16 is a pneumoprotein secreted by the non-ciliated epithelial club cells; thus, predominantly localised to the peripheral airways. Increased leakage of CC16 in the bloodstream and a rise in urinary excretion of CC16 have been reported after strenuous exercise and dry air hyperpnoea in athletes, supporting the role of high ventilation in inducing airway epithelial injury. That the CC16 increase in urine is blunted and bronchoconstriction blocked when the exercise is performed in warm humid air further suggests that warm humid air breathing is beneficial, not only to prevent EIB, but also to limit the degree of injury to the airways. Thus, wherever possible, athletes should be recommended to exercise in warm humid environments.
Reconstituted 2D Cell and Tissue Models
Published in Anthony J. Hickey, Sandro R.P. da Rocha, Pharmaceutical Inhalation Aerosol Technology, 2019
Nicole Schneider-Daum, Patrick Carius, Justus C. Horstmann, Claus-Michael Lehr
Mucus, which mainly consists of water (~95%), the high molecular glycoprotein mucin (~2%–5%), as well as low concentrations of lipids forms a hydrogel that lines the upper conducting airways (Boegh and Nielsen 2015). Through its mesh-like network, mucus traps particulate matter or microorganisms which are then transported to the pharynx via synchronized cilia movement in a process termed “mucociliary clearance.” Along the ramifications of the conducting airways, a columnar ciliated epithelium lines the bronchioles with several club cells and scattered goblet cells. Club cells show a non-ciliated, cuboidal morphology with a dome-shaped apical cell surface, and they secrete high levels of secretoglobins (Reynolds et al. 2002). The bronchioles develop into respiratory bronchioles with repeated ramifying of the bronchial tree, then transform into the pulmonary acinus.
Respiratory System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Tom P. McKevitt, David J. Lewis
Club cells are the progenitor cell of the terminal and respiratory bronchioles, and following epithelial damage, they can self-renew and give rise to ciliated cells. Keratinocyte growth factor is a potent club cell mitogen in rats (Fehrenbach et al. 2002).
Hypoxic conditions promote a proliferative, poorly differentiated phenotype in COPD lung tissue progenitor cells in vitro
Published in Experimental Lung Research, 2023
Tina P. Dale, Michael D. Santer, Mohammed Haris, Wei Zuo, Nicholas R. Forsyth
The levels of differentiation markers MUC5AC, MUC5B, and CC10 were quantitatively examined at the gene expression level, along with TP63 expression, in donor 1 cells. Expression of the cilia marker β IV tubulin was not included as we have commonly observed its widespread expression in the cytoplasm of cells in poorly differentiated cultures (Figure 2A), therefore an increase in a message cannot be correlated with successful differentiation. Both mucins were significantly upregulated in comparison to their undifferentiated counterparts (Figures 6A and 6B) with higher expression in 2% expanded cells compared to 21% which reached statistical significance (P ≤ 0.05) for MUC5B. Similarly, the club cell marker CC10 was also significantly upregulated by differentiation (Figure 6C). Interestingly, expression of the progenitor cell marker TP63 (Figure 6D) was not seen to decrease as a result of the differentiation process. 21% O2 expanded cells had a small and insignificant increase over expression levels in undifferentiated cells following differentiation at 21%, but 2% expanded cell cultures had a moderate and statistically significant (p ≤ 0.001) upregulation in expression compared to their undifferentiated counterparts. This, therefore, resulted in a significant difference between the 2% and 21% expanded cell groups following differentiation (P ≤ 0.05).
Inorganic chloramines: a critical review of the toxicological and epidemiological evidence as a basis for occupational exposure limit setting
Published in Critical Reviews in Toxicology, 2020
Gunilla Wastensson, Kåre Eriksson
Pneumoproteins, serum proteins especially produced in the respiratory tract, such as club cell protein 16 kDa (CC16) and surfactant-associated proteins (SP-A, SP-B and SP-D), have been suggested as biomarkers of the hyperpermeability that occurs in the deep lung (Bernard et al. 2005). CC16 is an anti-inflammatory protein secreted by club cells (formerly called Clara cells) in the airways and predominantly in terminal bronchioles from where it leaks into serum (Bernard and Lauwerys 1995). SP-A is the major surfactant-associated protein mainly secreted by alveolar type II cells and is considered to collaborate with SP-B and SP-C to spread and stabilize the phospholipid layer at the alveolar surface and thus reduce the surface tension (Hermans and Bernard 1999). CC16 and SP-A are largely, and SP-B exclusively, confined to the lungs, whereas SP-D is expressed by a number of tissues (Hermans et al. 2003). Small amounts of CC16, SP-A, SP-B and SP-D occur in blood, and these pneumoproteins have been validated as blood markers of lung hyperpermeability in a variety of lung disorders caused by different lung toxicants (Hermans and Bernard 1998). CC16 can also be used as a peripheral marker of the integrity of club cells (Hermans et al. 1999).
Pneumoproteins and markers of inflammation and platelet activation in the blood of grain dust exposed workers
Published in Biomarkers, 2018
Anne Straumfors, Wijnand Eduard, Kari K. Heldal, Marit Skogstad, Lars Barregård, Dag G. Ellingsen
The pathological response to grain dust exposure suggests activation of inflammatory and allergic pathways, although exact mechanisms are not completely elucidated. The non-ciliated bronchial epithelial club cells play an important role in protecting the lung from inhaled toxicants. One of the major proteins secreted by the club cells is the anti-inflammatory club cell-16 protein (CC-16) (Dierynck et al.1995, Lakind et al.2007). Serum levels of CC-16 are mainly affected by its production rate by club cells into the alveolar lavage fluid, the rate of diffusion from alveolar fluid into the serum, which is affected by permeability of the pulmonary epithelial barrier, and renal clearance (Lakind et al.2007). Inhalation of particles may affect this basic control, reducing the serum CC-16 by inhibiting, injuring or killing the club cells or increasing the concentration by inducing increased secretion and/or permeability. The CC-16 protein has been suggested to be a sensitive marker for detecting early permeability changes in the lung epithelial barrier and/or to evaluate the integrity of the club cells (Broeckaert and Bernard 2000). Reduced levels of serum CC-16 have been associated with cigarette smoking (Bernard et al.1994, Robin et al.2002). In contrast, acute or repeated exposures to bioaerosols in wastewater workers (Heldal et al.2013) (Steiner et al.2005) have been associated with increased serum CC-16 levels.