Allergy and Airway: Asthma III |

TLR2 Promotes Allergic Airway Inflammation Through JNK Signaling Pathway With Activation of Autophagy FREE TO VIEW

Lei Fang; Rongyu Liu, PhD
Author and Funding Information

Institute of Respiratory Disease, The First Affiliated Hospital of Anhui Medical University, Hefei, China

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

Chest. 2016;149(4_S):A28. doi:10.1016/j.chest.2016.02.030
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SESSION TYPE: Original Investigation Poster

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

PURPOSE: Toll-like receptors (TLRs) family as one of the best-characterized PRR families contributes to the pathogenesis of pulmonary diseases. Furthermore, autophagy such an immune process has been reported to be associated with asthma. Although numerous studies indicate that TLR2 activation led to contradictory effects in asthma, the role of TLR2 in OVA-induced mice model of asthma and the relationship with autophagy are little known.

METHODS: Wild-type and TLR2-/- mice were subjected to an allergic airway inflammation model. SP600125, a specific JNK inhibitor, was intraperitoneally administered in mice to study its effects on airway inflammatory responses. Inflammatory and autophagic molecular expression in lung tissues was detected by Western blot analysis.

RESULTS: In our study, increased expression of TLR2 was found in OVA-challenged lung tissues. TLR2-/- mice treated with OVA exhibited decreased serum OVA-specific IgE, airway inflammation, and goblet cell metaplasia compared with OVA-challenged WT mice. Meanwhile, the level of inflammatory and autophagic signaling activation was lower in OVA-treated TLR2-/- versus WT mice. OVA-induced JNK activation was also reduced in TLR2-/- mice. Interestingly, inhibition of JNK by SP600125 in WT mice similarly attenuated the level of serum OVA-specific IgE, OVA-induced airway inflammation and goblet cell metaplasia but not found in TLR2-/- mice in comparision with vehicle-treated TLR2-/- mice. At the same time, JNK inhibition affected inflammatory and autophagic signaling activation to some extent.

CONCLUSIONS: Collectively, in allergic airway disease, TLR2 might contribute to the maintenance of inflammatory disorder accompanying with activation of autophagy which JNK signaling may participate in.

CLINICAL IMPLICATIONS: This study may provide an important signal target for prevention of airway allergic inflammation.

DISCLOSURE: The following authors have nothing to disclose: Lei Fang, Rongyu Liu

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