Oxygen dose responsiveness of human fetal airway smooth muscle cells

Oxygen dose responsiveness of human fetal airway smooth muscle cells.

Maintenance of blood oxygen saturation dictates supplemental oxygen administration to premature infants, but hyperoxia predisposes survivors to respiratory diseases such as asthma. Although much research has focused on oxygen effects on alveoli in the setting of bronchopulmonary dysplasia, the mechanisms by which oxygen affects airway structure or function relevant to asthma are still under inv...

Oxygen regulates mitogen-stimulated proliferation of fetal human airway smooth muscle cells.

Increased airway smooth muscle (ASM) content is characteristic of infants with chronic lung disease of prematurity/bronchopulmonary dysplasia. Oxygen therapy, reactive oxygen species (ROS), and immature antioxidant defenses are major risk factors in chronic lung disease of prematurity/bronchopulmonary dysplasia, but their interrelationship is unclear. The direct effects of raised Po2 and modula...

Airway Responsiveness Lymphocytes: Role in Induction of Altered Airway Smooth Muscle Cells and T Bi-Directional Activation Between Human

TLR 3 Activation Increases Chemokine Expression in 1 Human Fetal Airway Smooth Muscle Cells

47 Viral infections, such as respiratory syncytial virus (RSV) and rhinovirus, adversely affect 48 neonatal and pediatric populations resulting in significant lung morbidity, including acute asthma 49 exacerbation. Studies in adults have demonstrated that human airway smooth muscle (ASM) 50 cells modulate inflammation through their ability to secrete inflammatory cytokines and 51 chemokines. Th...

Human Airway Smooth Muscle Cell