Triggering receptor expressed on myeloid cells and 5'adenosine monophosphate-activated protein kinase in the inflammatory response: a potential therapeutic target.
The events in the cellular and molecular signaling triggered during inflammation mitigate tissue healing. The metabolic check-point control mediated by 5'-adenosine monophosphate-activated protein kinase (AMPK) is crucial for switching the cells into an activated state capable of mediating inflammatory events. The cell metabolism involved in the inflammatory response represents a potential therapeutic target for the pharmacologic management of inflammation. Areas covered: In this article, a critical review is presented on triggering receptor expressed on myeloid cell (TREM) receptors and their role in the inflammatory responses, as well as homeostasis between different TREM molecules and their regulation. Additionally, we discussed the relationship between TREM and AMPK to identify novel targets to limit the inflammatory response. Literature search was carried out from the National Library of Medicine's Medline database (using PubMed as the search engine) and Google Scholar and identified relevant studies up to 30 March 2016 using inflammation, TREM, AMPK, as the key words. Expert commentary: The prevention of phenotype switching of immune cells during inflammation by targeting AMPK and TREM-1 could be beneficial for developing novel management strategies for inflammation and associated complications.
a Departments of Clinical & Translational Science , Creighton University School of Medicine , Omaha , NE , USA.
Finosh G
FG
Thankam
b Orthopedic Surgery , Creighton University School of Medicine , Omaha , NE , USA.
Matthew F
MF
Dilisio
a Departments of Clinical & Translational Science , Creighton University School of Medicine , Omaha , NE , USA.
Kaitlin A
KA
Dougherty
c Pathology , Creighton University School of Medicine , Omaha , NE , USA.
Nicholas E
NE
Dietz
a Departments of Clinical & Translational Science , Creighton University School of Medicine , Omaha , NE , USA.
Devendra K
DK
Agrawal
D055372:AMP-Activated Protein Kinases / Q000037:antagonists & inhibitors*; D000249:Adenosine Monophosphate / Q000378:metabolism; D000818:Animals; D006801:Humans; D007165:Immunosuppression Therapy; D007249:Inflammation / Q000188:drug therapy*; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors*; D058990:Molecular Targeted Therapy; D022423:Myeloid Cells / Q000187:drug effects* / Q000276:immunology; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D011971:Receptors, Immunologic / Q000037:antagonists & inhibitors*; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
D008562:Membrane Glycoproteins; D047428:Protein Kinase Inhibitors; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D000249:Adenosine Monophosphate; D055372:AMP-Activated Protein Kinases
5′-adenosine monophosphate-activated protein kinase; Immune cells; Inflammation; Triggering receptor expressed on myeloid cells; cell metabolism