Exposure to cockroach allergen (CRE) can lead to allergic airway inflammation. Autophagy is an evolutionarily conserved catabolic process in response to oxidative stress generated as a consequence of exposure to environmental allergens or toxicants. We aim to investigate the role of autophagy in mediating environmental CRE-induced lung inflammation and asthma.
The role of autophagy in the inception of allergic inflammation was investigated in our well-established mouse model of asthma. Markers of autophagy was evaluated by qPCR, Western blot, and immunofluorescent in the lung of CRE-treated mice and human epithelial cell line (A549).
Compared to control mice, CRE-treated mice had increased levels of autophagy by the increased expression of the autophagy markers LC3b-II, beclin-1, and Atg5 and deceased expression of p62 by qPCR and western blot.We also found significantly increased levels of LC3 by immunofluorescent in CRE-challenged mice compared with controls. Furthermore, inhibition of autophagy in CRE-induced mouse model of asthma, by the administration of Chloroquine (CLQ), showed decreased inflammatory lung infiltrates, mucus cell hyperplasia, Th2 cytokines in BAL fluid, and serum IgG1 and IgE. CLQ-treated mice also had decreased autophagy as assessed by qPCR. Interestingly, Human epithelial cell (A549) treated with CRE also showed increased in autophagy markers.
Our findings suggested that autophagy is involved in pathologies of allergen-induced lung inflammation.