Abstract：
:The resolution phase of acute inflammation is essential for tissue homeostasis, yet the underlying mechanisms remain unclear. We demonstrate that resolution of inflammation involves interactions between CD38 and tristetraprolin (TTP). During the onset of acute inflammation, CD38 levels are increased, leading to the production of Ca2+-signaling messengers, nicotinic acid adenine dinucleotide phosphate (NAADP), ADP ribose (ADPR), and cyclic ADPR (cADPR) from NAD(P)+. To initiate the onset of resolution, TTP expression is increased by the second messengers, NAADP and cADPR, which downregulate CD38 expression. The activation of TTP by Sirt1-dependent deacetylation, in response to increased NAD+ levels, suppresses the acute inflammatory response and decreases Rheb expression, inhibits mTORC1, and induces autophagolysosomes for bacterial clearance. TTP may represent a mechanistic target of anti-inflammatory agents, such as carbon monoxide. TTP mediates crosstalk between acute inflammation and autophagic clearance of bacteria from damaged tissue in the resolution of inflammation during sepsis.
journal_name
Cell Repjournal_title
Cell reportsauthors
Joe Y,Chen Y,Park J,Kim HJ,Rah SY,Ryu J,Cho GJ,Choi HS,Ryter SW,Park JW,Kim UH,Chung HTdoi
10.1016/j.celrep.2019.12.090subject
Has Abstractpub_date
2020-01-28 00:00:00pages
1063-1076.e5issue
4issn
2211-1247pii
S2211-1247(19)31755-3journal_volume
30pub_type
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