Findings from National Institute of Agrobiological Sciences Provide New Insights into Macrophages [Purinergic signaling via P2X(7) receptor mediates IL-1 beta production in Kupffer cells exposed to silica nanoparticle]
By a News Reporter-Staff News Editor at Health & Medicine Week -- Current study results on Macrophages have been published. According to news originating from Ibaraki, Japan, by NewsRx correspondents, research stated, "There is extensive evidence that nanoparticles (NPs) cause adverse effects in multiple organs, including liver, though the mechanisms involved remain to be fully established. Kupffer cells are macrophages resident in the liver, and play important roles in liver inflammation induced by various toxic agents, including lipopolysaccharide (LPS)."
Our news journalists obtained a quote from the research from the National Institute of Agrobiological Sciences, "Interleukin-1 (IL-1) family members IL-1 alpha,beta are released from LPS-primed macrophages exposed to NPs, including silica NPs (SNPs), via activation of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 inflammasomes. Here, we investigated the mechanism of production of IL-1 beta via activation of inflammasomes in mouse Kupffer cell line KUP5, focusing on the role of purinergic signaling via P2X(7) receptor. IL-1 beta production by LPS-primed KUP5 cells exposed to SNPs was increased dose-dependently, and was greatest in response to SNPs with a diameter of 30 nm (SNP30), as compared with 70-nm and 300-nm SNPs (SNP70 and SNP300). ATP release was also highest in cells exposed to SNP30. Treatment of LPS-primed KUP5 cells with ATP also induced a high level of IL-1 beta production, similar to that induced by SNP30. IL-1 beta production was significantly inhibited by apyrase (an ecto-nucleotidase) and A438079 (a P2X(7) antagonist/ATP-release inhibitor). Production of reactive oxygen species (ROS) was confirmed in cells exposed to SNP30."
According to the news editors, the research concluded: "ATP released from P2X(7) receptor in response to stimulation of KUP5 cells with SNP30 induces ROS production via cell-membrane NADPH oxidase. The ROS causes activation of inflammasomes, leading to caspase-1-dependent processing of IL-1 beta."
For more information on this research see: Purinergic signaling via P2X(7) receptor mediates IL-1 beta production in Kupffer cells exposed to silica nanoparticle. Toxicology, 2014;321():13-20. Toxicology can be contacted at: Elsevier Ireland Ltd, Elsevier House, Brookvale Plaza, East Park Shannon, Co, Clare, 00000, Ireland. (Elsevier - www.elsevier.com; Toxicology - www.elsevier.com/wps/product/cws_home/505518)
The news correspondents report that additional information may be obtained from S. Kojima, Natl Inst Agrobiol Sci, Transgen Anim Res Center, Tsuuba, Ibaraki 3058634, Japan. Additional authors for this research include Y. Negishi, M. Tsukimoto, T. Takenouchi, H. Kitani and K. Takeda (see also Macrophages).
Keywords for this news article include: Ibaraki, Japan, Asia, Emerging Technologies, Hemic and Immune Systems, Immunology, Kupffer Cells, Macrophages, Mononuclear Phagocyte System, Nanotechnology, Phagocytes, Silicon Nanocrystals
Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2014, NewsRx LLC