Allergy and Airway: Asthma II |

Chemical Chaperones Reverses Autophagic Dysfunction Resulting From Bronchial Asthma in the Lung Tissues of OVA-OVA Mice via Modulating NF-κB Activation FREE TO VIEW

Bo Zhou
Author and Funding Information

The First Affiliated Hospital of Xi’an Jiaotong University, Xi'an, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A17. doi:10.1016/j.chest.2016.02.019
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SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Chemical chaperones has been considered as an important regulator of bronchial asthma by improving airway inflammation, however the mechanism of chemical chaperones involved in insulin resistance remains not fully understood. In the present study, we investigated the effect of chemical chaperones (4-phenylbutyric acid, 4-PBA) on autophagy secondary to bronchial asthma in the lung tissues of OVA-OVA mice and in bronchial epithelial cell models, and clarified the intracellular events responsible for chemical chaperones-mediated effects.

METHODS: Chemical chaperones was administered in OVA-OVA mice and in tunicamycin-induced mouse bronchial epithelial cells, and autophagy markers and nuclear factor-κB (NF-κB) signaling molecular were assessed via real-time PCR and western blot.

RESULTS: The injections of chemical chaperones (4-PBA) in OVA-OVA mice exhibited down-regulation of inflammatory cytokines and airway hyperresponsiveness, and improved airway inflammation compared with OVA-OVA mice receiving vehicle. Meanwhile, the administration of chemical chaperones (4-PBA) not only reversed autophagic dysfunction, but also modulated NF-κB signaling in lung tissues of OVA-OVA mice. In accordance with these findings in vivo, 4-PBA treatment also had a protective impact in bronchial epithelial cell in the presence of tunicamycin by regulation of mammalian target of rapamycin (mTOR) and NF-κB signaling.

CONCLUSIONS: Chemical chaperones inhibit autophagy and improves airway inflammation in the lung tissues of OVA-OVA Mice and in bronchial epithelial cell models via modulating NF-κB activation, which may be a promising therapeutic strategies of bronchial asthma.

CLINICAL IMPLICATIONS: We investigate the role of autophagy in improved airway inflammation of bronchial asthma by chemical chaperones and offer novel opportunities for treatment of bronchial asthma.

DISCLOSURE: The following authors have nothing to disclose: Bo Zhou

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