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Staphylococcus aureus supernatant induces the release of mouse β-defensin-14 from osteoblasts via the p38 MAPK and NF-κB pathways

  • Authors:
    • Chen Zhu
    • Hui Qin
    • Tao Cheng
    • Hong-Lue Tan
    • Yong-Yuan Guo
    • Si-Feng Shi
    • De-Sheng Chen
    • Xian-Long Zhang

  • View Affiliations

  • Published online on: April 15, 2013     https://doi.org/10.3892/ijmm.2013.1346
  • Pages: 1484-1494
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Abstract

Mammalian β-defensins are small cationic peptides of approximately 2-6 kDa that have been implicated in mediating innate immune defenses against microbial infection. Previous studies have reported that mouse β-defensin-14 (MBD‑14), based on structural and functional similarities, appears to be an ortholog of human β-defensin-3 (HBD-3). The aim of this study was to identify the signaling pathways that contribute to the expression of MBD-14 in mouse osteoblasts (OBs) upon contact with methicillin-resistant Staphylococcus aureus (S. aureus) supernatant (SAS) to provide a theoretical basis for the use of MDB-14 as a therapeutic agent in the treatment of intramedullary infection with S. aureus in vivo. The bacterial exoproducts released by S. aureus mainly include a large amount of enterotoxins. Using mouse OBs, the release and regulation of MBD-14 was evaluated by real-time polymerase chain reaction (PCR) and enzyme‑linked immunosorbent assay (ELISA) following exposure to SAS. The activation of the p38 mitogen‑activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB) pathways was determined by western blot analysis. OBs treated with lipopolysaccharide (LPS) were used as the positive control. The results revealed that SAS significantly promoted the phosphorylation of p38 MAPK, NF-κB and the inhibitory subunit of NF-κBα (IκBα) in a time-dependent manner. The treatment of OBs with SB203580 (an inhibitor of p38 MAPK) and pyrrolidine dithiocarbamate (PDTC, an inhibitor of NF-κB) prior to stimulation with SAS significantly inhibited the phosphorylation and mRNA expression of p38 MAPK and NF-κB p65, simultaneously reducing the release of MBD-14. Our findings suggest that the release of MBD-14 is mediated at least in part through the activation of p38 MAPK and NF-κB in response to S. aureus‑secreted bacterial exoproducts. Moreover, our data demonstrate the innate immune capacity of OBs under conditions of bacterial challenge to enhance the local expression of this MBD-14, a peptide with anti‑staphylococcal activity.
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June 2013
Volume 31 Issue 6

Print ISSN: 1107-3756
Online ISSN:1791-244X

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  • Journal Metrics
  • Impact Factor: 5.7
  • Ranked Medicine Research and Experimental
    (total number of cites)
  • CiteScore: 12.3
  • CiteScore Rank: Q1: #28/347 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 1.022
  • SCImago Journal Rank (SJR): 1.167
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Spandidos Publications style
Zhu C, Qin H, Cheng T, Tan H, Guo Y, Shi S, Chen D and Zhang X: Staphylococcus aureus supernatant induces the release of mouse β-defensin-14 from osteoblasts via the p38 MAPK and NF-κB pathways. Int J Mol Med 31: 1484-1494, 2013.
APA
Zhu, C., Qin, H., Cheng, T., Tan, H., Guo, Y., Shi, S. ... Zhang, X. (2013). Staphylococcus aureus supernatant induces the release of mouse β-defensin-14 from osteoblasts via the p38 MAPK and NF-κB pathways. International Journal of Molecular Medicine, 31, 1484-1494. https://doi.org/10.3892/ijmm.2013.1346
MLA
Zhu, C., Qin, H., Cheng, T., Tan, H., Guo, Y., Shi, S., Chen, D., Zhang, X."Staphylococcus aureus supernatant induces the release of mouse β-defensin-14 from osteoblasts via the p38 MAPK and NF-κB pathways". International Journal of Molecular Medicine 31.6 (2013): 1484-1494.
Chicago
Zhu, C., Qin, H., Cheng, T., Tan, H., Guo, Y., Shi, S., Chen, D., Zhang, X."Staphylococcus aureus supernatant induces the release of mouse β-defensin-14 from osteoblasts via the p38 MAPK and NF-κB pathways". International Journal of Molecular Medicine 31, no. 6 (2013): 1484-1494. https://doi.org/10.3892/ijmm.2013.1346