Abstract
Background Activation of neutrophils sequestered in the alveolar milieu can cause the release of reactive oxygen species (ROS), increasingly regarded as key substances modulating epithelium dysfunction and disruption. These oxidants are generated by the neutrophil respiratory burst oxidase system that reduces molecular oxygen (O2) to superoxide (O2-). Alpha-1 antitrypsin (AAT) deficiency (AATD) provides us with the most definitive evidence for the physiological and clinical importance of AAT and in this study we examined the immunomodulatory activity of AAT and investigated whether neutrophil ROS production was regulated by AAT.
Highlights
Activation of neutrophils sequestered in the alveolar milieu can cause the release of reactive oxygen species (ROS), increasingly regarded as key substances modulating epithelium dysfunction and disruption
Alpha-1 antitrypsin regulates neutrophil reactive oxygen species production via inhibition of key players of the respiratory burst oxidase system
Alpha-1 antitrypsin (AAT) deficiency (AATD) provides us with the most definitive evidence for the physiological and clinical importance of AAT and in this study we examined the immunomodulatory activity of AAT and investigated whether neutrophil ROS production was regulated by AAT
Summary
Activation of neutrophils sequestered in the alveolar milieu can cause the release of reactive oxygen species (ROS), increasingly regarded as key substances modulating epithelium dysfunction and disruption. These oxidants are generated by the neutrophil respiratory burst oxidase system that reduces molecular oxygen (O2) to superoxide (O2-). Alpha-1 antitrypsin (AAT) deficiency (AATD) provides us with the most definitive evidence for the physiological and clinical importance of AAT and in this study we examined the immunomodulatory activity of AAT and investigated whether neutrophil ROS production was regulated by AAT
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