| Heme oxygenase-1 signals are involved in preferential inhibition of pro-inflammatory cytokine release by surfactin in cells activated with Porphyromonas gingivalis lipopolysaccharide. | |
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MedLine Citation:
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PMID: 20833156 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Porphyromonas gingivalis is considered the major pathogen of periodontal disease, which leads to chronic inflammation in oral tissues. P. gingivalis-produced lipopolysaccharide (LPS) is a key factor in the development of periodontitis. It is established that surfactin produced by Bacillus subtilis confers anti-inflammatory properties. However, the underlying mechanisms responsible for surfactin-induced anti-inflammatory actions in the context of periodontitis are poorly understood. In this study, we investigated whether surfactin affected P. gingivalis LPS-induced pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-12, and determined that it significantly inhibited their production. Surfactin-mediated inhibition was mainly due to blocked activation of P. gingivalis LPS-triggered nuclear factor-κB. We also examined whether the regulatory effect of surfactin on P. gingivalis LPS-stimulated human THP-1 macrophages was mediated by the induction of heme oxygenase-1 (HO-1) signals, and determined that surfactin also induced HO-1 mRNA and protein expression via activation of Nrf-2. Additionally, we found that small interfering RNA-mediated knock-down of Nrf-2 significantly inhibited surfactin-induced HO-1 expression. Furthermore, inhibition of phosphoinositide 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK) significantly decreased surfactin-induced HO-1 expression, which is consistent with the suggestion that surfactin-induced HO-1 expression occurs via PI3K/Akt, ERK, and Nrf-2. Treatment with a selective inhibitor of HO-1 reversed the surfactin-mediated inhibition of pro-inflammatory cytokines, suggesting that surfactin induces anti-inflammatory effects by activating Nrf-2-mediated HO-1 induction via PI3K/Akt and ERK signaling. Collectively, these observations support the potential of surfactin as a candidate in strategies to prevent caries, periodontitis, or other inflammatory diseases. |
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Authors:
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Sun Young Park; Young Hun Kim; Eun-Kyoung Kim; Eun Yeon Ryu; Sang-Joon Lee |
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Publication Detail:
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Type: Journal Article Date: 2010-09-15 |
Journal Detail:
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Title: Chemico-biological interactions Volume: 188 ISSN: 1872-7786 ISO Abbreviation: Chem. Biol. Interact. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-12 Completed Date: 2010-12-21 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0227276 Medline TA: Chem Biol Interact Country: Ireland |
Other Details:
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Languages: eng Pagination: 437-45 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier Ireland Ltd. All rights reserved. |
Affiliation:
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Pusan National University, Busan, Republic of Korea. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Active Transport, Cell Nucleus
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drug effects Cell Line Cell Nucleus / drug effects, metabolism Cytokines / secretion* Enzyme Activation / drug effects Enzyme Induction / drug effects Extracellular Signal-Regulated MAP Kinases / metabolism Heme Oxygenase-1 / biosynthesis, genetics, metabolism* Humans Inflammation / metabolism, pathology Lipopeptides / pharmacology* Lipopolysaccharides / pharmacology* Macrophages / cytology, drug effects*, metabolism, secretion NF-E2-Related Factor 2 / metabolism NF-kappa B / metabolism Peptides, Cyclic / pharmacology* Porphyromonas gingivalis / chemistry* Proto-Oncogene Proteins c-akt / metabolism RNA, Messenger / genetics, metabolism Signal Transduction / drug effects* Up-Regulation / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Lipopeptides; 0/Lipopolysaccharides; 0/NF-E2-Related Factor 2; 0/NF-kappa B; 0/Peptides, Cyclic; 0/RNA, Messenger; 24730-31-2/surfactin peptide; EC 1.14.99.3/Heme Oxygenase-1; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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