Overexpression of peroxiredoxin 6 protect mice from ovalbumin-induced airway inflammation and hypersecretion of MUC5AC by reducing ROS levels

Background: Oxidative stress plays an important role in the pathogenesis of asthma. Peroxiredoxin 6 (Prdx 6), as a newly identified peroxidase, protect cell or organ from reactive oxygen species (ROS)-induced oxidative stress. Objective: The present study aimed at investigating the involvement of prdx 6 in asthma. Methods: The ovalbumin (OVA) - induced allergic airway inflammation and MUC5AC production were examined in wild-type (WT), overexpressing (Prdx 6+/+) or Prdx6 null (Prdx 6–/–) mice. Prdx 69s expression in lung and intracellular ROS levels in bronchoalveolar lavage fluid (BALF) were evaluated. Results: The expression of Prdx 6 was reduced significantly and up-regulated by dexamethasone and ambroxol in lung from WT mice. Prdx 6+/+ mice had significantly low airway inflammation, low levels of IL-13 in BALF as compared with those in WT mice. In addition, lower expression of MUC5AC in airway epithelial cells, less secretion of MUC5AC in BALF were found in Prdx6+/+ model mice, especially with fewer intracellular ROS levels in BALF. However, Prdx6–/– mice showed no significant difference compared to WT mice. Conclusions: Our data indicate that overexpression of Prdx 6 prevent allergic airway inflammation and hypersecretion by reducing ROS levels. While due to several compensatory mechanisms, targeted disruption of Prdx 6 fails to increase OVA-induced asthma.