Journal of Autoimmunity丨NAD+依赖性SIRT5通过促进 p65 的乙酰化来逆转内毒素耐受

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Chestnut Studying       摘要  The induction and persistence of a hypo-inflammatory and immunosuppressive state in severe sepsis is commonly associated with increased risks of secondary infections and mortality. Toll-like receptor (TLR)-triggered inflammatory response of macrophages/monocytes plays an important role in determining the outcome of hyper-inflammation during the acute phase and the hypo-inflammation during immunosuppressive phase of sepsis. However, the mechanisms for controlling hypo-inflammatory response in endotoxin tolerant macrophages remain to be fully understood. Considering that metabolic control of inflammation is an emerging field and the balance between AMP/ATP and oxidized NAD+/reduced NADH is associated with inflammation and metabolism, we analyzed the level of NAD+ in TLR-triggered innate inflammatory response, and found that the decreased level of NAD+ was significantly related to the increased inflammatory cytokine production both in vivo and in vitro ………………………………