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Allergy and Airway: Asthma IV |

IL-33 Promotes Airway Remodeling in Asthma Through ST2/ERK1/2/MSK1 Signal Pathway FREE TO VIEW

Liang Dong, PhD
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Qilu Hospital of Shandong University, Jinan, China


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


Chest. 2016;149(4_S):A36. doi:10.1016/j.chest.2016.02.038
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SESSION TITLE: Asthma IV

SESSION TYPE: Original Investigation Poster

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

PURPOSE: Interleukin-33 (IL-33) dysregulation plays a critical role in the pathogenesis of asthma airway inflammation and remodeling. However, the cellular and molecular mechanisms of IL-33 in asthma remodeling remain unclear.

METHODS: Expression of IL-33 and ST2 was examined in lung specimens from patients with asthma using immunohischemical analysis. Human lung fibroblasts were pretreated with anti-ST2 antibody, U0126 and H89 respectively and then treated with IL-33 recombination protein. Then western blot, cell immunofluorescence and real-time quantitative PCR were used to determine the activation of extracellular signal-regulated protein kinase 1/2 (ERK1/2) and mitogen- and stress-activated protein kinase 1 (MSK1) and the expression of alpha smooth muscle actin (α-SMA) and collagen I. In addition, the effect of soluble ST2 (sST2) was tested in a mouse asthma model to determine if IL-33 blocking influences airway remodeling of asthma.

RESULTS: We found that expression of IL-33 and ST2 was upregulated in airway samples from patients with asthma. Furthermore, we showed in vitro that IL-33 induced α-SMA and collagen I expression via ST2-ERK1/2-MSK1 signaling pathway in human lung fibroblast. Using a mouse asthma model, we demonstrated that IL-33 neutralization by administration of sST2 inhibited IL-33/ST2-ERKI/2-MSK1signaling pathway and airway remodeling in vivo.

CONCLUSIONS: In conclusion, these data indicate that IL-33, binding with its receptor ST2, can induce α-SMA and collagens I expression in human lung fibroblast through ERK1/2/MSK1 signaling pathway.

CLINICAL IMPLICATIONS: IL-33 blocking by sST2 overcomes ovalbumin (OVA)-induced airway remodeling in vivo and may serve as a new therapeutic option for asthma.

DISCLOSURE: The following authors have nothing to disclose: Liang Dong

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