UMass Chan Affiliations
UMass Metabolic NetworkDepartment of Medicine, Division of Gastroenterology
Graduate School of Biomedical Sciences, Translational Science Program
Document Type
Letter to the EditorPublication Date
2017-11-20
Metadata
Show full item recordAbstract
Much controversy surrounds the pathogenesis of acetaminophen-induced inflammation. Acetaminophen (APAP) is a well-studied xenobiotic that in high doses results in a deadly, yet preventable, form of liver failure. Although its effects are sudden and often irreversible, its mechanism is far from simple. In fact, at first glance, recent studies seem to refute each other. The field has been grappling with seemingly contradictory results driven mainly by often-generalized assumptions and different experimental systems. As always, the devil—or in this case, liver failure—is in the details. In this paper, Tang and colleagues identified macrophage-derived interleukin (IL)-1α as a mediator of sterile inflammation in a mouse model of APAP hepatotoxicity. IL-1α is an alarmin that unlike IL-1β, is constitutively expressed in many cells as a precursor. IL-1α precursor (pre-IL-1α) is active as a damage-associated molecular pattern (DAMP). After enzymatic cleavage, mature IL-1α can signal a more potent pro-inflammatory message.Source
Cell Mol Immunol. 2017 Nov 20. pii: cmi2017108. doi: 10.1038/cmi.2017.108. Link to article on publisher's siteDOI
10.1038/cmi.2017.108Permanent Link to this Item
http://hdl.handle.net/20.500.14038/36621PubMed ID
29151582Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1038/cmi.2017.108