About: Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice

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About: Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice
Creator	Coban, Sahin Furi, Istvan Szabo, Gyongyi Tornai, David Shen, Zu Sigalov, Alexander
Source	Medline; PMC
abstract	Alcoholic liver disease (ALD) is characterized by macrophage and neutrophil leukocyte recruitment and activation in the liver. Damage‐ and pathogen‐associated molecular patterns contribute to a self‐perpetuating proinflammatory state in ALD. Triggering receptor expressed on myeloid cells 1 (TREM‐1) is a surface receptor that amplifies inflammation induced by toll‐like receptors (TLRs) and is expressed on neutrophils and monocytes/macrophages. We hypothesized that TREM‐1 signaling contributes to proinflammatory pathway activation in ALD. Using an in vivo ALD model in mice, we tested the effects of ligand‐independent TREM‐1 inhibitory peptides that were formulated into human high‐density lipoprotein (HDL)‐mimicking complexes GF9‐HDL and GA/E31‐HDL. As revealed in vitro, macrophages endocytosed these rationally designed complexes through scavenger receptors. A 5‐week alcohol feeding with the Lieber‐DeCarli diet in mice resulted in increased serum alanine aminotransferase (ALT), liver steatosis, and increased proinflammatory cytokines in the liver. TREM‐1 messenger RNA (mRNA) expression was significantly increased in alcohol‐fed mice, and TREM‐1 inhibitors significantly reduced this increase. TREM‐1 inhibition significantly attenuated alcohol‐induced spleen tyrosine kinase (SYK) activation, an early event in both TLR4 and TREM‐1 signaling. The TREM‐1 inhibitors significantly inhibited macrophage (epidermal growth factor‐like module‐containing mucin‐like hormone receptor‐like 1 [F4/80], clusters of differentiation [CD]68) and neutrophil (lymphocyte antigen 6 complex, locus G [Ly6G] and myeloperoxidase [MPO]) markers and proinflammatory cytokines (monocyte chemoattractant protein 1 [MCP‐1], tumor necrosis factor α [TNF‐α], interleukin‐1β [IL‐1β], macrophage inflammatory protein 1α [MIP‐1α]) at the mRNA level compared to the HDL vehicle. Administration of TREM‐1 inhibitors ameliorated liver steatosis and early fibrosis markers (α‐smooth muscle actin [αSMA] and procollagen1α [Pro‐Col1α]) at the mRNA level in alcohol‐fed mice. However, the HDL vehicle also reduced serum ALT and some cytokine protein levels in alcohol‐fed mice, indicating HDL‐related effects. Conclusion: HDL‐delivered novel TREM‐1 peptide inhibitors ameliorate early phases of inflammation and neutrophil and macrophage recruitment and activation in the liver and attenuate hepatocyte damage and liver steatosis. TREM‐1 inhibition represents a promising therapeutic approach for further investigations in ALD.
has issue date	2018-10-29(xsd:dateTime)
bibo:doi	10.1002/hep4.1269
bibo:pmid	30619998
has license	cc-by-nc-nd
sha1sum (hex)	fe2b70a4317057c021120d2281f2d7796c742e86
schema:url	https://doi.org/10.1002/hep4.1269
resource representing a document's title	Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice
has PubMed Central identifier	PMC6312652
has PubMed identifier	30619998
schema:publication	Hepatol Commun
resource representing a document's body	covid:fe2b70a4317057c021120d2281f2d7796c742e86#body_text
is schema:about of	named entity 'TRIGGERING RECEPTOR EXPRESSED ON MYELOID CELLS 1' named entity 'DIET' named entity 'USING' named entity 'MACROPHAGE' named entity 'INCREASE' named entity 'INDEPENDENT' named entity 'SELF' named entity 'SURFACE' named entity 'MODEL' named entity 'INCREASED SERUM ALANINE' named entity 'SPLEEN TYROSINE KINASE' named entity 'NEUTROPHIL LEUKOCYTE' named entity 'HUMAN' named entity 'INFLAMMATION' named entity 'SCAVENGER RECEPTORS' named entity 'IN VIVO' named entity 'SIGNALING' named entity 'COMPLEXES' named entity 'EXPRESSION' named entity 'FED' named entity 'RECEPTOR' named entity 'REDUCED' named entity 'proinflammatory' named entity 'HDL' named entity 'liver' named entity 'diet' named entity 'mice' named entity 'signaling' named entity 'MACROPHAGE' named entity 'NEUTROPHIL ACTIVATION' named entity 'STATE' named entity 'ALCOHOL' named entity 'PEPTIDES' named entity 'MICE' named entity 'FEEDING' named entity 'LIGAND' named entity 'TOLL-LIKE RECEPTORS' named entity 'EFFECTS' named entity 'NEUTROPHILS' named entity 'INCREASED' named entity 'INDUCED' named entity 'INFLAMMATION' named entity 'INHIBITION' named entity 'AMELIORATES' named entity 'ALCOHOLIC LIVER DISEASE' named entity 'TLR4' named entity 'HIGH-DENSITY LIPOPROTEIN' named entity 'HDL' named entity 'CHARACTERIZED' named entity 'PATHOGEN' named entity 'IS A' named entity 'ALCOHOLIC LIVER DISEASE' named entity 'MONOCYTES' named entity 'IN VITRO' named entity 'ALANINE AMINOTRANSFERASE' named entity 'PATTERNS' named entity 'ATTENUATED' named entity 'MOLECULAR' named entity 'EARLY' named entity 'CONTRIBUTE ' named entity 'MESSENGER RNA' named entity 'MACROPHAGES' named entity 'ASSOCIATED' named entity 'LEUKOCYTE RECRUITMENT' named entity 'REVEALED' named entity 'PATHWAY' named entity 'PROINFLAMMATORY CYTOKINES' named entity 'EXPRESSED' named entity 'THESE' named entity 'INHIBITORY' named entity 'ACTIVATION' named entity 'EVENT' named entity 'INHIBITORS' named entity 'DAMAGE' named entity 'TESTED' named entity 'LIVER'

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