570:
Cockroach-induced lung inflammation is associated with increased autophagy
Sunday, March 4, 2018
South Hall A2 (Convention Center)
Xin Zhang, MD, Danh C. Do, PhD, Pei-song Gao
RATIONALE:

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.

METHODS:

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).

RESULTS:

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.

CONCLUSIONS:

Our findings suggested that autophagy is involved in pathologies of allergen-induced lung inflammation.