A Static Magnetic Field Reduces lipopolysaccharide-induced Proinflammatory Cytokine Levels of Fibroblasts by Altering Membrane Fluidity

Che-Tong Lin, Chi-An Chen, Yu-Fu Chen, Chun-Yang Chen, Sheng-Yang Lee, Haw-Ming Huang

Research output: Contribution to journalArticle

Abstract

Lipopolysaccharide (LPS) is one of the major substances that initiate an immune host response in microbial infections which results in cytotoxicity. In terms of the treatment of the immune response, much research on endotoxin tolerance that can reduce LPS-induced damages has been conducted. In this experiment, cultured fibroblasts were challenged with LPS in order to initiate an inflammatory reaction. Cell numbers and various proinflammatory cytokine levels were compared between a static magnetic field (SMF)-exposed group and an unexposed group. Our results showed that with LPS challenge, fibroblasts exposed to a 4000-G SMF demonstrated a higher cell density (8.28±0.14 10^4 cells/ml) when compared to the unexposed (control) group (4.5±0.16 10^4 cells/ml, p<0.05). Meanwhile, levels of LPS-induced interleukin-1β and tumor necrosis factor-α in the SMF-exposed groups were significantly lower at 32.9% and 61.4% than those of the unexposed counterparts, respectively (p<0.05). The change in the fluorescence anisotropy of TMA-DPH increased when cells were exposed to SMF. These results indicate that a static magnetic field may decrease LPS-induced proinflammatory cytokine levels by altering the membrane fluidity.
Original languageEnglish
Pages (from-to)11-18
Number of pages8
JournalJournal of Dental Sciences
Volume2
Issue number1
Publication statusPublished - 2007

Fingerprint

Membrane Fluidity
Magnetic Fields
Lipopolysaccharides
Fibroblasts
Cytokines
Cell Count
Fluorescence Polarization
Interleukin-1
Endotoxins
Tumor Necrosis Factor-alpha
Control Groups
Infection
Research

Keywords

  • static magnetic field
  • fibroblast
  • lipopolysaccharide
  • proinflammatory cytokine
  • membrane fluidity

Cite this

A Static Magnetic Field Reduces lipopolysaccharide-induced Proinflammatory Cytokine Levels of Fibroblasts by Altering Membrane Fluidity. / Lin, Che-Tong; Chen, Chi-An; Chen, Yu-Fu; Chen, Chun-Yang; Lee, Sheng-Yang; Huang, Haw-Ming.

In: Journal of Dental Sciences, Vol. 2, No. 1, 2007, p. 11-18.

Research output: Contribution to journalArticle

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abstract = "Lipopolysaccharide (LPS) is one of the major substances that initiate an immune host response in microbial infections which results in cytotoxicity. In terms of the treatment of the immune response, much research on endotoxin tolerance that can reduce LPS-induced damages has been conducted. In this experiment, cultured fibroblasts were challenged with LPS in order to initiate an inflammatory reaction. Cell numbers and various proinflammatory cytokine levels were compared between a static magnetic field (SMF)-exposed group and an unexposed group. Our results showed that with LPS challenge, fibroblasts exposed to a 4000-G SMF demonstrated a higher cell density (8.28±0.14 10^4 cells/ml) when compared to the unexposed (control) group (4.5±0.16 10^4 cells/ml, p<0.05). Meanwhile, levels of LPS-induced interleukin-1β and tumor necrosis factor-α in the SMF-exposed groups were significantly lower at 32.9{\%} and 61.4{\%} than those of the unexposed counterparts, respectively (p<0.05). The change in the fluorescence anisotropy of TMA-DPH increased when cells were exposed to SMF. These results indicate that a static magnetic field may decrease LPS-induced proinflammatory cytokine levels by altering the membrane fluidity.",
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AU - Lin, Che-Tong

AU - Chen, Chi-An

AU - Chen, Yu-Fu

AU - Chen, Chun-Yang

AU - Lee, Sheng-Yang

AU - Huang, Haw-Ming

PY - 2007

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N2 - Lipopolysaccharide (LPS) is one of the major substances that initiate an immune host response in microbial infections which results in cytotoxicity. In terms of the treatment of the immune response, much research on endotoxin tolerance that can reduce LPS-induced damages has been conducted. In this experiment, cultured fibroblasts were challenged with LPS in order to initiate an inflammatory reaction. Cell numbers and various proinflammatory cytokine levels were compared between a static magnetic field (SMF)-exposed group and an unexposed group. Our results showed that with LPS challenge, fibroblasts exposed to a 4000-G SMF demonstrated a higher cell density (8.28±0.14 10^4 cells/ml) when compared to the unexposed (control) group (4.5±0.16 10^4 cells/ml, p<0.05). Meanwhile, levels of LPS-induced interleukin-1β and tumor necrosis factor-α in the SMF-exposed groups were significantly lower at 32.9% and 61.4% than those of the unexposed counterparts, respectively (p<0.05). The change in the fluorescence anisotropy of TMA-DPH increased when cells were exposed to SMF. These results indicate that a static magnetic field may decrease LPS-induced proinflammatory cytokine levels by altering the membrane fluidity.

AB - Lipopolysaccharide (LPS) is one of the major substances that initiate an immune host response in microbial infections which results in cytotoxicity. In terms of the treatment of the immune response, much research on endotoxin tolerance that can reduce LPS-induced damages has been conducted. In this experiment, cultured fibroblasts were challenged with LPS in order to initiate an inflammatory reaction. Cell numbers and various proinflammatory cytokine levels were compared between a static magnetic field (SMF)-exposed group and an unexposed group. Our results showed that with LPS challenge, fibroblasts exposed to a 4000-G SMF demonstrated a higher cell density (8.28±0.14 10^4 cells/ml) when compared to the unexposed (control) group (4.5±0.16 10^4 cells/ml, p<0.05). Meanwhile, levels of LPS-induced interleukin-1β and tumor necrosis factor-α in the SMF-exposed groups were significantly lower at 32.9% and 61.4% than those of the unexposed counterparts, respectively (p<0.05). The change in the fluorescence anisotropy of TMA-DPH increased when cells were exposed to SMF. These results indicate that a static magnetic field may decrease LPS-induced proinflammatory cytokine levels by altering the membrane fluidity.

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