Publication detail

The unique role of dietary l-arginine in the acceleration of peritoneal macrophage sensitivity to bacterial endotoxin

PEKAROVÁ, M. KUCHTA, R. KADLEC, J.

Original Title

The unique role of dietary l-arginine in the acceleration of peritoneal macrophage sensitivity to bacterial endotoxin

English Title

The unique role of dietary l-arginine in the acceleration of peritoneal macrophage sensitivity to bacterial endotoxin

Type

journal article in Web of Science

Language

en

Original Abstract

It is known that cells and organisms can indirectly sense changes in l-arginine availability via changes in the activity of various metabolic pathways. However, the mechanism(s) by which genes can be directly regulated by l-arginine in mammalian cells have not yet been elucidated. We investigated the effect of l-arginine in the in vivo model of peritoneal inflammation in mice and in vitro in RAW 264.7 macrophages. A detailed analysis of basic physiological functions and selected intracellular signaling cascades revealed that l-arginine is crucial for the acceleration of macrophage activation by bacterial lipopolysaccharide. l-arginine increased the production of reactive oxygen species, nitric oxide, release of Ca2+, as well as inducible nitric oxide synthase expression. Interestingly, the effect of l-arginine on macrophage activation was dependent on the phosphorylation of mitogen-activated protein kinases and activity of phospholipase C. In RAW 264.7 cells, l-arginine was shown to modulate the response of macrophages toward lipopolysaccharide via the activation of G-protein-coupled receptors. According to our data, we concluded that l-arginine availability plays a key role in the initiation of intracellular signaling pathways that trigger the lipopolysaccharide-induced inflammatory responses in murine macrophages. Although macrophages are partially stimulated in the absence of extracellular l-arginine, the presence of this amino acid significantly accelerates the sensitivity of macrophages to bacterial endotoxin.

English abstract

It is known that cells and organisms can indirectly sense changes in l-arginine availability via changes in the activity of various metabolic pathways. However, the mechanism(s) by which genes can be directly regulated by l-arginine in mammalian cells have not yet been elucidated. We investigated the effect of l-arginine in the in vivo model of peritoneal inflammation in mice and in vitro in RAW 264.7 macrophages. A detailed analysis of basic physiological functions and selected intracellular signaling cascades revealed that l-arginine is crucial for the acceleration of macrophage activation by bacterial lipopolysaccharide. l-arginine increased the production of reactive oxygen species, nitric oxide, release of Ca2+, as well as inducible nitric oxide synthase expression. Interestingly, the effect of l-arginine on macrophage activation was dependent on the phosphorylation of mitogen-activated protein kinases and activity of phospholipase C. In RAW 264.7 cells, l-arginine was shown to modulate the response of macrophages toward lipopolysaccharide via the activation of G-protein-coupled receptors. According to our data, we concluded that l-arginine availability plays a key role in the initiation of intracellular signaling pathways that trigger the lipopolysaccharide-induced inflammatory responses in murine macrophages. Although macrophages are partially stimulated in the absence of extracellular l-arginine, the presence of this amino acid significantly accelerates the sensitivity of macrophages to bacterial endotoxin.

Keywords

Macrophages; l-arginine; Lipopolysaccharide; Mitogen-activated protein kinases; Phospholipase C; G-protein-coupled receptor

RIV year

2013

Released

27.11.2012

Publisher

PublisherSpringer-Verlag

Pages from

2443

Pages to

2457

Pages count

12

BibTex


@article{BUT95688,
  author="Michaela {Pekarová} and Radek {Kuchta} and Jaroslav {Kadlec} and Zdeňka {Kuchtová}",
  title="The unique role of dietary l-arginine in the acceleration of peritoneal macrophage sensitivity to bacterial endotoxin",
  annote="It is known that cells and organisms can indirectly sense changes in l-arginine availability via changes in the activity of various metabolic pathways. However, the mechanism(s) by which genes can be directly regulated by l-arginine in mammalian cells have not yet been elucidated. We investigated the effect of l-arginine in the in vivo model of peritoneal inflammation in mice and in vitro in RAW 264.7 macrophages. A detailed analysis of basic physiological functions and selected intracellular signaling cascades revealed that l-arginine is crucial for the acceleration of macrophage activation by bacterial lipopolysaccharide. l-arginine increased the production of reactive oxygen species, nitric oxide, release of Ca2+, as well as inducible nitric oxide synthase expression. Interestingly, the effect of l-arginine on macrophage activation was dependent on the phosphorylation of mitogen-activated protein kinases and activity of phospholipase C. In RAW 264.7 cells, l-arginine was shown to modulate the response of macrophages toward lipopolysaccharide via the activation of G-protein-coupled receptors. According to our data, we concluded that l-arginine availability plays a key role in the initiation of intracellular signaling pathways that trigger the lipopolysaccharide-induced inflammatory responses in murine macrophages. Although macrophages are partially stimulated in the absence of extracellular l-arginine, the presence of this amino acid significantly accelerates the sensitivity of macrophages to bacterial endotoxin.",
  address="PublisherSpringer-Verlag",
  chapter="95688",
  institution="PublisherSpringer-Verlag",
  number="11",
  volume="2012",
  year="2012",
  month="november",
  pages="2443--2457",
  publisher="PublisherSpringer-Verlag",
  type="journal article in Web of Science"
}