ABSTRACT
House dust mite (HDM) is one of the significant causes for airway inflammation such as asthma. It induces oxidative stress and an inflammatory response in the lungs through the release of chemokines such as interleukin-8 (IL-8). Reactive oxygen species (ROS) activate inflammatory signaling mediators such as mitogen-activated protein kinases (MAPKs) and redox-sensitive transcription factors including NF-κB and AP-1. Ascorbic acid shows an antioxidant and anti-inflammatory activities in various cells. It ameliorated the symptoms of HDM-induced rhinitis. The present study was aimed to investigate whether HDM could induce IL-8 expression through activation of MAPKs, NF-κB, and AP-1 and whether ascorbic acid could inhibit HDM-stimulated IL-8 expression by reducing ROS and suppressing activation of MAPKs, NF-κB, and AP-1 in respiratory epithelial H292 cells. H292 cells were treated with HDM (5 μg/mL) in the absence or presence of ascorbic acid (100 or 200 μM). HDM treatment increased ROS levels, and activated MAPKs, NF-κB, and AP-1 and thus, induced IL-8 expression in H292 cells. Ascorbic acid reduced ROS levels and inhibited activation of MAPKs, NF-κB and AP-1 and L-8 expression in H292 cells. In conclusion, consumption of ascorbic acid-rich foods may be beneficial for prevention of HDM-mediated respiratory inflammation by suppressing oxidative stress-mediated MAPK signaling pathways and activation of NF-kB and AP-1.
ABSTRACT
House dust mite (HDM) is one of the significant causes for airway inflammation such as asthma. It induces oxidative stress and an inflammatory response in the lungs through the release of chemokines such as interleukin-8 (IL-8). Reactive oxygen species (ROS) activate inflammatory signaling mediators such as mitogen-activated protein kinases (MAPKs) and redox-sensitive transcription factors including NF-κB and AP-1. Ascorbic acid shows an antioxidant and anti-inflammatory activities in various cells. It ameliorated the symptoms of HDM-induced rhinitis. The present study was aimed to investigate whether HDM could induce IL-8 expression through activation of MAPKs, NF-κB, and AP-1 and whether ascorbic acid could inhibit HDM-stimulated IL-8 expression by reducing ROS and suppressing activation of MAPKs, NF-κB, and AP-1 in respiratory epithelial H292 cells. H292 cells were treated with HDM (5 μg/mL) in the absence or presence of ascorbic acid (100 or 200 μM). HDM treatment increased ROS levels, and activated MAPKs, NF-κB, and AP-1 and thus, induced IL-8 expression in H292 cells. Ascorbic acid reduced ROS levels and inhibited activation of MAPKs, NF-κB and AP-1 and L-8 expression in H292 cells. In conclusion, consumption of ascorbic acid-rich foods may be beneficial for prevention of HDM-mediated respiratory inflammation by suppressing oxidative stress-mediated MAPK signaling pathways and activation of NF-kB and AP-1.