Effects of E-Cigs on Physiological Pathways and Proposed Therapeutic Intervention with Bixin.

Electronic cigarettes (e-cigs) have increased in popularity and usage over the last few decades. There is rising concern regarding the long-term effects of e-cigs on human health, considering their relatively recent introduction to the market. E-cigs are generally composed of a liquid containing nicotine and various chemicals, a battery, a vaporization chamber, and a coil that serves to heat the liquid upon inhalation of the mouthpiece.

Bio-MOFs Based on Natural Phenolic, Hematoxylin Leverages Biomedical Applications: Enzyme Inhibition, Antioxidant, and Antibacterial Properties.

Here, using natural hematoxylin (HT) as linker, metal-organic frameworks (MOFs) from Cu(II), Fe(II), and Fe(III) ions was prepared. The SEM images and DLS analyses revealed HT-based MOFs are View Article and Find Full Text PDF

Co-inhibition of CD73 and ADORA2B Improves Long-Term Cigarette Smoke Induced Lung Injury.

Adenosine (ADO) involvement in lung injury depends on the activation of its receptors. The ADO A receptor (ADORA2A) and A receptor (ADORA2B) are best described to have both tissue-protective and tissue-destructive processes. However, no approach has been effective in delineating the mechanism(s) involved with ADO shifting from its tissue-protective to tissue-destructive properties in chronic airway injury.

Influence of Cigarettes and Alcohol on the Severity and Death of COVID-19: A Multicenter Retrospective Study in Wuhan, China.

Background: The recent emergence and rapid global spread of coronavirus disease 2019 (COVID-19) is leading to public health crises worldwide. Alcohol consumption and cigarette smoking (CS) are two known risk factors in many diseases including respiratory infections.

Methods: We performed a multi-center study in the four largest hospitals designated for COVID-19 patients in Wuhan.

Cigarette Smoke Impairs A Adenosine Receptor Mediated Wound Repair through Up-regulation of Duox-1 Expression.

Cigarette smoke (CS) exposure and intrinsic factors such as the NADPH oxidases produce high levels of reactive oxygen species (ROS), ensuing inflammatory tissue injury. We previously demonstrated that CS-generated ROS, particularly hydrogen peroxide (HO), impaired adenosine stimulated wound repair. We hypothesized that CS exposure modulates expression of Dual oxidase 1 (Duox-1), a NADPH oxidases known to generate HO.

NLRP3 deletion protects from hyperoxia-induced acute lung injury.

Inspiration of a high concentration of oxygen, a therapy for acute lung injury (ALI), could unexpectedly lead to reactive oxygen species (ROS) production and hyperoxia-induced acute lung injury (HALI). Nucleotide-binding domain and leucine-rich repeat PYD-containing protein 3 (NLRP3) senses the ROS, triggering inflammasome activation and interleukin-1β (IL-1β) production and secretion. However, the role of NLRP3 inflammasome in HALI is unclear.

Smoke extract impairs adenosine wound healing: implications of smoke-generated reactive oxygen species.

Adenosine concentrations are elevated in the lungs of patients with asthma and chronic obstructive pulmonary disease, where it balances between tissue repair and excessive airway remodeling. We previously demonstrated that the activation of the adenosine A2A receptor promotes epithelial wound closure. However, the mechanism by which adenosine-mediated wound healing occurs after cigarette smoke exposure has not been investigated.

Co-exposure to cigarette smoke and alcohol decreases airway epithelial cell cilia beating in a protein kinase Cε-dependent manner.

Alcohol use disorders are associated with increased lung infections and exacerbations of chronic lung diseases. Whereas the effects of cigarette smoke are well recognized, the interplay of smoke and alcohol in modulating lung diseases is not clear. Because innate lung defense is mechanically maintained by airway cilia action and protein kinase C (PKC)-activating agents slow ciliary beat frequency (CBF), we hypothesized that the combination of smoke and alcohol would decrease CBF in a PKC-dependent manner.

The p38 mitogen-activated protein kinases modulate endothelial cell survival and tissue repair.

Objective And Design: This study is designed to investigate the role of p38 MAPK in modulating human pulmonary artery endothelial cells (HPAECs) survival and tissue repair functions.

Methods: HPAECs (passage 8-12) were used for all experiments. Cells were treated with IL-1β (0.

Adenosine activation of A(2B) receptor(s) is essential for stimulated epithelial ciliary motility and clearance.

Mucociliary clearance, vital to lung clearance, is dependent on cilia beat frequency (CBF), coordination of cilia, and the maintenance of periciliary fluid. Adenosine, the metabolic breakdown product of ATP, is an important modulator of ciliary motility. However, the contributions of specific adenosine receptors to key airway ciliary motility processes are unclear.

Ethanol blocks adenosine uptake via inhibiting the nucleoside transport system in bronchial epithelial cells.

Background: Adenosine uptake into cells by nucleoside transporters plays a significant role in governing extracellular adenosine concentration. Extracellular adenosine is an important signaling molecule that modulates many cellular functions via 4 G-protein-coupled receptor subtypes (A(1), A(2A), A(2B), and A(3)). Previously, we demonstrated that adenosine is critical in maintaining airway homeostasis and airway repair and that airway host defenses are impaired by alcohol.

Adenosine promotion of cellular migration in bronchial epithelial cells is mediated by the activation of cyclic adenosine monophosphate-dependent protein kinase A.

Migration of neighboring cells into the injury is important for rapid repair of damaged airway epithelium. We previously reported that activation of the A(2A )receptors (A(2A)ARs) mediates adenosine-stimulated epithelial wound healing, suggesting a role for adenosine in migration. Because A(2A)AR increases cyclic adenosine monophosphate (cAMP) levels in many cells, we hypothesized that cAMP-dependent protein kinase A (PKA) is involved in adenosine-mediated cellular migration.

Hog barn dust slows airway epithelial cell migration in vitro through a PKCalpha-dependent mechanism.

Agricultural work and other occupational exposures are responsible for approximately 15% of chronic obstructive pulmonary disease (COPD). COPD involves airway remodeling in response to chronic lung inflammatory events and altered airway repair mechanisms. However, the effect of agricultural dust exposure on signaling pathways that regulate airway injury and repair has not been well characterized.

Cigarette smoke extract increases C5a receptor expression in human bronchial epithelial cells.

We have shown that exposing human bronchial epithelial cells (HBECs) to 5% cigarette smoke extract (CSE) up-regulates C5a anaphylatoxin receptor (C5aR) expression as determined by flow cytometric analysis and immunohistochemistry. In this study, we conducted whole-cell saturation studies to quantitate the receptor number. After exposing an HBEC line (BEAS-2B) to CSE, radiolabeled C5a bound saturably with Kd = 2.