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IL-22 Up-Regulates β-Defensin-2 Expression in Human Alveolar Epithelium via STAT3 but Not NF-κB Signaling Pathway

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Abstract

Human β-defensin-2(HBD-2) is one of the two major vertebrate antimicrobial peptide families (α and β), which is highly expressed by proinflammatory induction in the lung and exhibit broad-spectrum antimicrobial activity. We observed that IL-22 receptors high expressed on the membrane of A549 cells; HBD-2 mRNA was expressed in a time- and concentration-dependent manners in A549 cells when treated with IL-22; further studies demonstrated that HBD-2 expression was attenuated by AG490, but to JSH-23, inhibitors of p-STAT3 DNA binding and NF-κB/ p65 subunit nuclear translocation, respectively. These results support that IL-22-mediated signalling pathway of HBD-2 gene expression involved STAT3 but not NF-κB in human alveolar epithelium. These findings provide a new insight into how IL-22 may play an important link between innate and adaptive immunity, thereby anti-infection locally in the alveolar epithelium.

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Abbreviations

IL:

Interleukin

HBD:

Human β-defensin

TBE:

Tracheobronchialepithelial

AMPs:

Antimicrobial peptides

IFN-γ:

Interferon-γ

GM-CSF:

Granulocyte-macrophage colony-stimulatingfactor

TNF-α:

Tumor necrosis factor α

PBS:

Phosphate-buffered saline

LPS:

Lipopolysaccharides

LAM:

Lipoarabinomannan

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Acknowledgments

We thank the Department of Oncology of the First Affiliated Hospital of Nanjing Medical University for providing alveolar epithelial type II cell lines A549 and Cui Ping Liu for expert technical help.

Conflict of Interest

None of the authors of this study has any financial or commercial conflicts of interest.

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Correspondence to Xuefan Cui.

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Li, A., Gan, Y., Wang, R. et al. IL-22 Up-Regulates β-Defensin-2 Expression in Human Alveolar Epithelium via STAT3 but Not NF-κB Signaling Pathway. Inflammation 38, 1191–1200 (2015). https://doi.org/10.1007/s10753-014-0083-z

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  • DOI: https://doi.org/10.1007/s10753-014-0083-z

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