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  • 1
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    Acetylcholine-synthesizing T cells relay neural signals in a vagus nerve circuit (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-17
    Description: Neural circuits regulate cytokine production to prevent potentially damaging inflammation. A prototypical vagus nerve circuit, the inflammatory reflex, inhibits tumor necrosis factor-alpha production in spleen by a mechanism requiring acetylcholine signaling through the alpha7 nicotinic acetylcholine receptor expressed on cytokine-producing macrophages. Nerve fibers in spleen lack the enzymatic machinery necessary for acetylcholine production; therefore, how does this neural circuit terminate in cholinergic signaling? We identified an acetylcholine-producing, memory phenotype T cell population in mice that is integral to the inflammatory reflex. These acetylcholine-producing T cells are required for inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter, acetylcholine, required to control innate immune responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548937/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosas-Ballina, Mauricio -- Olofsson, Peder S -- Ochani, Mahendar -- Valdes-Ferrer, Sergio I -- Levine, Yaakov A -- Reardon, Colin -- Tusche, Michael W -- Pavlov, Valentin A -- Andersson, Ulf -- Chavan, Sangeeta -- Mak, Tak W -- Tracey, Kevin J -- R01 GM057226/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 7;334(6052):98-101. doi: 10.1126/science.1209985. Epub 2011 Sep 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921156" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*biosynthesis ; Action Potentials ; Animals ; CD4-Positive T-Lymphocytes/*immunology/*metabolism ; Choline O-Acetyltransferase/metabolism ; Cholinergic Agents/metabolism ; Female ; *Immunity, Innate ; Immunologic Memory ; Inflammation ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; *Neuroimmunomodulation ; Norepinephrine/pharmacology ; Receptors, Nicotinic/metabolism ; Signal Transduction ; Spleen/immunology/innervation/metabolism ; T-Lymphocyte Subsets/immunology/metabolism ; Tumor Necrosis Factor-alpha/blood ; Vagus Nerve/*physiology ; Vagus Nerve Stimulation ; alpha7 Nicotinic Acetylcholine Receptor
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Novel role of PKR in inflammasome activation and HMGB1 release (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-18
    Description: The inflammasome regulates the release of caspase activation-dependent cytokines, including interleukin (IL)-1beta, IL-18 and high-mobility group box 1 (HMGB1). By studying HMGB1 release mechanisms, here we identify a role for double-stranded RNA-dependent protein kinase (PKR, also known as EIF2AK2) in inflammasome activation. Exposure of macrophages to inflammasome agonists induced PKR autophosphorylation. PKR inactivation by genetic deletion or pharmacological inhibition severely impaired inflammasome activation in response to double-stranded RNA, ATP, monosodium urate, adjuvant aluminium, rotenone, live Escherichia coli, anthrax lethal toxin, DNA transfection and Salmonella typhimurium infection. PKR deficiency significantly inhibited the secretion of IL-1beta, IL-18 and HMGB1 in E. coli-induced peritonitis. PKR physically interacts with several inflammasome components, including NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3), NLRP1, NLR family CARD domain-containing protein 4 (NLRC4), absent in melanoma 2 (AIM2), and broadly regulates inflammasome activation. PKR autophosphorylation in a cell-free system with recombinant NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC, also known as PYCARD) and pro-caspase-1 reconstitutes inflammasome activity. These results show a crucial role for PKR in inflammasome activation, and indicate that it should be possible to pharmacologically target this molecule to treat inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163918/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163918/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Ben -- Nakamura, Takahisa -- Inouye, Karen -- Li, Jianhua -- Tang, Yiting -- Lundback, Peter -- Valdes-Ferrer, Sergio I -- Olofsson, Peder S -- Kalb, Thomas -- Roth, Jesse -- Zou, Yongrui -- Erlandsson-Harris, Helena -- Yang, Huan -- Ting, Jenny P-Y -- Wang, Haichao -- Andersson, Ulf -- Antoine, Daniel J -- Chavan, Sangeeta S -- Hotamisligil, Gokhan S -- Tracey, Kevin J -- DK052539/DK/NIDDK NIH HHS/ -- G0700654/Medical Research Council/United Kingdom -- R01 DK052539/DK/NIDDK NIH HHS/ -- R01 GM057226/GM/NIGMS NIH HHS/ -- R01 GM062508/GM/NIGMS NIH HHS/ -- R01 GM62508/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Aug 30;488(7413):670-4. doi: 10.1038/nature11290.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA. blu@nshs.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22801494" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Adenosine Triphosphate/pharmacology ; Animals ; Antigens, Bacterial/pharmacology ; Apoptosis Regulatory Proteins/metabolism ; Bacterial Toxins/pharmacology ; CARD Signaling Adaptor Proteins/metabolism ; Calcium-Binding Proteins/metabolism ; Carrier Proteins/metabolism ; Cell Line ; Cells, Cultured ; Crystallins/metabolism ; Escherichia coli/immunology/physiology ; Escherichia coli Infections/immunology/metabolism ; Female ; HMGB1 Protein/blood/*secretion ; Humans ; Inflammasomes/agonists/*metabolism ; Interleukin-18/blood ; Interleukin-1beta/blood ; Interleukin-6/analysis/blood ; Macrophages, Peritoneal/drug effects/metabolism ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Peritonitis/metabolism ; Phosphorylation ; RNA, Double-Stranded/immunology/pharmacology ; Rotenone/pharmacology ; Salmonella Infections/immunology/metabolism ; Salmonella typhimurium/immunology/physiology ; Transfection ; Uric Acid/pharmacology ; eIF-2 Kinase/antagonists & inhibitors/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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