Vasopressin inhibits endotoxin binding in activated macrophages

Ya Ying Chang, Chen Hsien Yang, Shih Ching Wang, Ming Chang Kao, Pei Shan Tsai, Chun Jen Huang

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background Vasopressin possesses potent anti-inflammatory effects. Endotoxin recognition (mediated by cluster of differentiation 14 [CD14]), endotoxin binding, and subsequent nuclear factor-κB (NF-κB) activation are essential mechanisms for initiation of the inflammatory response. We elucidated the effects of vasopressin on these essential mechanisms of inflammation with the hypothesis that vasopressin could inhibit CD14 expression, endotoxin binding, and NF-κB activation in activated macrophages. Methods Murine macrophage-like cell line RAW264.7 cells were stimulated with endotoxin (lipopolysaccharide [LPS]; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL; designated as the LPS and the LPS + V groups, respectively). After reaction, between-group differences in inflammatory molecule concentrations and levels of NF-κB activation, endotoxin-macrophages binding, and CD14 expression were compared. Analysis of variance was performed for statistical analysis. Results The concentrations of chemokine macrophage inflammatory protein 2 and cytokine interleukin 6 of the LPS + V group were significantly lower than those of the LPS group (P = 0.004 and P <0.001). The nuclear concentration of phosphorylated NF-κB p65 and cytosolic concentration of phosphorylated inhibitor-κBα of the LPS + V group were significantly lower than those of the LPS group (all P <0.05). In addition, the level of endotoxin-macrophages binding of the LPS + V group was significantly lower than that of the LPS group (P <0.001). The level of surface CD14 expression of the LPS + V group was also significantly lower than that of the LPS group (P = 0.019). Conclusions This study confirmed the potent anti-inflammatory effects of vasopressin. The mechanisms underlying the anti-inflammatory effects of vasopressin may involve its effects on inhibiting CD14 expression, endotoxin binding, and subsequent NF-κB activation.

Original languageEnglish
Pages (from-to)412-418
Number of pages7
JournalJournal of Surgical Research
Volume197
Issue number2
DOIs
Publication statusPublished - Aug 1 2015

Fingerprint

Vasopressins
Endotoxins
Lipopolysaccharides
Macrophages
Anti-Inflammatory Agents
Chemokine CXCL2
Macrophage Activation
Chemokines
Interleukin-6
Analysis of Variance
Cytokines
Inflammation
Cell Line

Keywords

  • CD14
  • Lipopolysaccharide
  • Nuclear factor-κB
  • Vasopressin

ASJC Scopus subject areas

  • Surgery

Cite this

Vasopressin inhibits endotoxin binding in activated macrophages. / Chang, Ya Ying; Yang, Chen Hsien; Wang, Shih Ching; Kao, Ming Chang; Tsai, Pei Shan; Huang, Chun Jen.

In: Journal of Surgical Research, Vol. 197, No. 2, 01.08.2015, p. 412-418.

Research output: Contribution to journalArticle

Chang, Ya Ying ; Yang, Chen Hsien ; Wang, Shih Ching ; Kao, Ming Chang ; Tsai, Pei Shan ; Huang, Chun Jen. / Vasopressin inhibits endotoxin binding in activated macrophages. In: Journal of Surgical Research. 2015 ; Vol. 197, No. 2. pp. 412-418.
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abstract = "Background Vasopressin possesses potent anti-inflammatory effects. Endotoxin recognition (mediated by cluster of differentiation 14 [CD14]), endotoxin binding, and subsequent nuclear factor-κB (NF-κB) activation are essential mechanisms for initiation of the inflammatory response. We elucidated the effects of vasopressin on these essential mechanisms of inflammation with the hypothesis that vasopressin could inhibit CD14 expression, endotoxin binding, and NF-κB activation in activated macrophages. Methods Murine macrophage-like cell line RAW264.7 cells were stimulated with endotoxin (lipopolysaccharide [LPS]; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL; designated as the LPS and the LPS + V groups, respectively). After reaction, between-group differences in inflammatory molecule concentrations and levels of NF-κB activation, endotoxin-macrophages binding, and CD14 expression were compared. Analysis of variance was performed for statistical analysis. Results The concentrations of chemokine macrophage inflammatory protein 2 and cytokine interleukin 6 of the LPS + V group were significantly lower than those of the LPS group (P = 0.004 and P <0.001). The nuclear concentration of phosphorylated NF-κB p65 and cytosolic concentration of phosphorylated inhibitor-κBα of the LPS + V group were significantly lower than those of the LPS group (all P <0.05). In addition, the level of endotoxin-macrophages binding of the LPS + V group was significantly lower than that of the LPS group (P <0.001). The level of surface CD14 expression of the LPS + V group was also significantly lower than that of the LPS group (P = 0.019). Conclusions This study confirmed the potent anti-inflammatory effects of vasopressin. The mechanisms underlying the anti-inflammatory effects of vasopressin may involve its effects on inhibiting CD14 expression, endotoxin binding, and subsequent NF-κB activation.",
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N2 - Background Vasopressin possesses potent anti-inflammatory effects. Endotoxin recognition (mediated by cluster of differentiation 14 [CD14]), endotoxin binding, and subsequent nuclear factor-κB (NF-κB) activation are essential mechanisms for initiation of the inflammatory response. We elucidated the effects of vasopressin on these essential mechanisms of inflammation with the hypothesis that vasopressin could inhibit CD14 expression, endotoxin binding, and NF-κB activation in activated macrophages. Methods Murine macrophage-like cell line RAW264.7 cells were stimulated with endotoxin (lipopolysaccharide [LPS]; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL; designated as the LPS and the LPS + V groups, respectively). After reaction, between-group differences in inflammatory molecule concentrations and levels of NF-κB activation, endotoxin-macrophages binding, and CD14 expression were compared. Analysis of variance was performed for statistical analysis. Results The concentrations of chemokine macrophage inflammatory protein 2 and cytokine interleukin 6 of the LPS + V group were significantly lower than those of the LPS group (P = 0.004 and P <0.001). The nuclear concentration of phosphorylated NF-κB p65 and cytosolic concentration of phosphorylated inhibitor-κBα of the LPS + V group were significantly lower than those of the LPS group (all P <0.05). In addition, the level of endotoxin-macrophages binding of the LPS + V group was significantly lower than that of the LPS group (P <0.001). The level of surface CD14 expression of the LPS + V group was also significantly lower than that of the LPS group (P = 0.019). Conclusions This study confirmed the potent anti-inflammatory effects of vasopressin. The mechanisms underlying the anti-inflammatory effects of vasopressin may involve its effects on inhibiting CD14 expression, endotoxin binding, and subsequent NF-κB activation.

AB - Background Vasopressin possesses potent anti-inflammatory effects. Endotoxin recognition (mediated by cluster of differentiation 14 [CD14]), endotoxin binding, and subsequent nuclear factor-κB (NF-κB) activation are essential mechanisms for initiation of the inflammatory response. We elucidated the effects of vasopressin on these essential mechanisms of inflammation with the hypothesis that vasopressin could inhibit CD14 expression, endotoxin binding, and NF-κB activation in activated macrophages. Methods Murine macrophage-like cell line RAW264.7 cells were stimulated with endotoxin (lipopolysaccharide [LPS]; 100 ng/mL) or LPS plus vasopressin (1000 pg/mL; designated as the LPS and the LPS + V groups, respectively). After reaction, between-group differences in inflammatory molecule concentrations and levels of NF-κB activation, endotoxin-macrophages binding, and CD14 expression were compared. Analysis of variance was performed for statistical analysis. Results The concentrations of chemokine macrophage inflammatory protein 2 and cytokine interleukin 6 of the LPS + V group were significantly lower than those of the LPS group (P = 0.004 and P <0.001). The nuclear concentration of phosphorylated NF-κB p65 and cytosolic concentration of phosphorylated inhibitor-κBα of the LPS + V group were significantly lower than those of the LPS group (all P <0.05). In addition, the level of endotoxin-macrophages binding of the LPS + V group was significantly lower than that of the LPS group (P <0.001). The level of surface CD14 expression of the LPS + V group was also significantly lower than that of the LPS group (P = 0.019). Conclusions This study confirmed the potent anti-inflammatory effects of vasopressin. The mechanisms underlying the anti-inflammatory effects of vasopressin may involve its effects on inhibiting CD14 expression, endotoxin binding, and subsequent NF-κB activation.

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KW - Nuclear factor-κB

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