scholarly journals P2‐20: Propylene glycol and glycerol, components of E‐cigarettes and heated tobacco products, damage epithelial cells in human airways

Respirology ◽  
2021 ◽  
Vol 26 (S3) ◽  
pp. 121-121
Keyword(s):  
Epithelial Cells ◽  
Propylene Glycol ◽  
Tobacco Products ◽  
Human Airways

scholarly journals Effects of Glycerol and Propylene Glycol on Smoke Release of Heat-not-burn Tobacco Products

2021 ◽  
Vol 1802 (2) ◽  
pp. 022025
Author(s):  
Yuxing Tong ◽  
Yimin Xiong ◽  
Qunshan Yan ◽  
Song Gao ◽  
Xi Le ◽  
...  
Keyword(s):  
Propylene Glycol ◽  
Tobacco Products

scholarly journals Increased transcription of cytokine genes in human lung epithelial cells through activation of a TRPM8 variant by cold temperatures

2008 ◽  
Vol 295 (1) ◽  
pp. L194-L200 ◽  
Author(s):  
Ashwini S. Sabnis ◽  
Christopher A. Reilly ◽  
John M. Veranth ◽  
Garold S. Yost
Keyword(s):  
Epithelial Cells ◽  
Human Lung ◽  
External Environment ◽  
Lung Epithelial Cells ◽  
Critical Element ◽  
Cold Temperatures ◽  
Cold Air ◽  
Lung Epithelial ◽  
Human Airways ◽  
Human Lung Epithelial Cells

Recognition of temperature is a critical element of sensory perception and allows mammals to evaluate both their external environment and internal status. The respiratory epithelium is constantly exposed to the external environment, and prolonged inhalation of cold air is detrimental to human airways. However, the mechanisms responsible for adverse effects elicited by cold air on the human airways are poorly understood. Transient receptor potential melastatin family member 8 (TRPM8) is a well-established cold- and menthol-sensing cation channel. We recently discovered a functional cold- and menthol-sensing variant of the TRPM8 ion channel in human lung epithelial cells. The present study explores the hypothesis that this TRPM8 variant mediates airway cell inflammatory responses elicited by cold air/temperatures. Here, we show that activation of the TRPM8 variant in human lung epithelial cells leads to increased expression of several cytokine and chemokine genes, including IL-1α, -1β, -4, -6, -8, and -13, granulocyte-macrophage colony-stimulating factor (GM-CSF), and TNF-α. Our results provide new insights into mechanisms that potentially control airway inflammation due to inhalation of cold air and suggest a possible role for the TRPM8 variant in the pathophysiology of asthma.

scholarly journals E-cigarette constituents propylene glycol and vegetable glycerin decrease glucose uptake and its metabolism in airway epithelial cells in vitro

2020 ◽  
Vol 319 (6) ◽  
pp. L957-L967
Author(s):  
M. Woodall ◽  
J. Jacob ◽  
K. K. Kalsi ◽  
V. Schroeder ◽  
E. Davis ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Glucose Uptake ◽  
Cell Volume ◽  
Propylene Glycol ◽  
Glucose Transport ◽  
Airway Epithelial Cells ◽  
Apical Surface ◽  
Airway Epithelial ◽  
Solute Permeability ◽  
Short Term Exposure

Electronic nicotine delivery systems, or e-cigarettes, utilize a liquid solution that normally contains propylene glycol (PG) and vegetable glycerin (VG) to generate vapor and act as a carrier for nicotine and flavorings. Evidence indicated these “carriers” reduced growth and survival of epithelial cells including those of the airway. We hypothesized that 3% PG or PG mixed with VG (3% PG/VG, 55:45) inhibited glucose uptake in human airway epithelial cells as a first step to reducing airway cell survival. Exposure of H441 or human bronchiolar epithelial cells (HBECs) to PG and PG/VG (30–60 min) inhibited glucose uptake and mitochondrial ATP synthesis. PG/VG inhibited glycolysis. PG/VG and mannitol reduced cell volume and height of air-liquid interface cultures. Mannitol, but not PG/VG, increased phosphorylation of p38 MAPK. PG/VG reduced transepithelial electrical resistance, which was associated with increased transepithelial solute permeability. PG/VG decreased fluorescence recovery after photobleaching of green fluorescent protein-linked glucose transporters GLUT1 and GLUT10, indicating that glucose transport function was compromised. Puffing PG/VG vapor onto the apical surface of primary HBECs for 10 min to mimic the effect of e-cigarette smoking also reduced glucose transport. In conclusion, short-term exposure to PG/VG, key components of e-cigarettes, decreased glucose transport and metabolism in airway cells. We propose that this was a result of PG/VG reduced cell volume and membrane fluidity, with further consequences on epithelial barrier function. Taking these results together, we suggest these factors contribute to reduced defensive properties of the epithelium. We propose that repeated/chronic exposure to these agents are likely to contribute to airway damage in e-cigarette users.

scholarly journals Tollip Inhibits ST2 Signaling in Airway Epithelial Cells Exposed to Type 2 Cytokines and Rhinovirus

2019 ◽  
Vol 12 (1) ◽  
pp. 103-115 ◽  
Author(s):  
Azzeddine Dakhama ◽  
Reem Al Mubarak ◽  
Nicole Pavelka ◽  
Dennis Voelker ◽  
Max Seibold ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Molecular Mechanisms ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Proinflammatory Response ◽  
Type 2 Cytokines ◽  
Cytokine Milieu ◽  
Human Airways

The negative immune regulator Tollip inhibits the proinflammatory response to rhinovirus (RV) infection, a contributor to airway neutrophilic inflammation and asthma exacerbations, but the underlying molecular mechanisms are poorly understood. Tollip may inhibit IRAK1, a signaling molecule downstream of ST2, the receptor of IL-33. This study was carried out to determine whether Tollip downregulates ST2 signaling via inhibition of IRAK1, but promotes soluble ST2 (sST2) production, thereby limiting excessive IL-8 production in human airway epithelial cells during RV infection in a type 2 cytokine milieu (e.g., IL-13 and IL-33 stimulation). Tollip- and IRAK1-deficient primary human tracheobronchial epithelial (HTBE) cells and Tollip knockout (KO) HTBE cells were generated using the shRNA knockdown and CRISPR/Cas9 approaches, respectively. Cells were stimulated with IL-13, IL-33, and/or RV16. sST2, activated IRAK1, and IL-8 were measured. A Tollip KO mouse model was utilized to test if Tollip regulates the airway inflammatory response to RV infection in vivo under IL-13 and IL-33 treatment. Following IL-13, IL-33, and RV treatment, Tollip-deficient (vs. -sufficient) HTBE cells produced excessive IL-8, accompanied by decreased sST2 production but increased IRAK1 activation. IL-8 production following IL-13/IL-33/RV exposure was markedly attenuated in IRAK1-deficient HTBE cells, as well as in Tollip KO HTBE cells treated with an IRAK1 inhibitor or a recombinant sST2 protein. Tollip KO (vs. wild-type) mice developed exaggerated airway neutrophilic responses to RV in the context of IL-13 and IL-33 treatment. Collectively, these data demonstrate that Tollip restricts excessive IL-8 production in type 2 cytokine-exposed human airways during RV infection by promoting sST2 production and inhibiting IRAK1 activation. sST2 and IRAK1 may be therapeutic targets for attenuating excessive neutrophilic airway inflammation in asthma, especially during RV infection.

Electronic cigarette liquid substances propylene glycol and vegetable glycerin induce an inflammatory response in gingival epithelial cells

2020 ◽  
Vol 40 (1) ◽  
pp. 25-34
Author(s):  
A Beklen ◽  
D Uckan
Keyword(s):  
Epithelial Cells ◽  
Propylene Glycol ◽  
Western Blotting ◽  
Electronic Cigarettes ◽  
Periodontal Diseases ◽  
Biological Response ◽  
Electronic Cigarette ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gingival Epithelial Cells

Information on the effects of propylene glycol (PG) and vegetable glycerin (VG) and on cytotoxicity and subsequent activation of the biological mediators is limited in periodontal diseases. This study analyzes the effect of unflavored PG/VG alone or in combination with nicotine on gingival epithelial cells. The cells were exposed to different PG/VG (± nicotine) concentrations for 24 h and cytotoxicity was evaluated by calorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromid assay. The expressions of interleukin (IL)-6, IL-8, and matrix metalloproteinases (MMPs)-9 were measured using an enzyme-linked immunosorbent assay and a western blotting. Stimulation with PG/VG mixtures reduced cell viability compared to nonexposed controls ( p < 0.05). Adding PG/VG increased the levels of IL-6, IL-8, and MMP-9, and the amount of PG had more biological impact compared to the VG amount. The nicotine augmented this effect compared to its nicotine-free counterparts. In western blotting result, MMP-9 was clearly activated in almost all samples. These findings suggest that the main constituents PG/VG are cytotoxic and able to induce biological response in gingival cells in vitro. Despite being advertised as less harmful than conventional cigarettes, electronic cigarette liquid pose certain risks on periodontal cells. Awareness about the effects of electronic cigarettes on periodontal diseases must be increased.

scholarly journals Expression and localization of COX-2 in human airways and cultured airway epithelial cells

1999 ◽  
Vol 13 (5) ◽  
pp. 999 ◽  
Author(s):  
D.N. Watkins ◽  
D.J. Peroni ◽  
C. Lenzo ◽  
D.A. Knight ◽  
M.J. Garlepp ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cox 2 ◽  
Human Airways

Exposure to acrolein disrupts the molecular regulation of mitochondrial metabolism in epithelial cells of the human airways

2021 ◽  
Vol 350 ◽  
pp. S167-S168
Author(s):  
C. Tulen ◽  
C.H. Schiffers ◽  
C. van de Wetering ◽  
H.W. Cremers ◽  
E. Duistermaat ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mitochondrial Metabolism ◽  
Molecular Regulation ◽  
Human Airways
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