• Xiao-Jing Wu, Hui Liang, Ying Zhang, Xu-Ming Yang, Hong-Yu Wang, Hui Li, Xin-Yi Li, Kai Chen, Yan-Lin Wang, Jian-Guo Li, Zong-Ze Zhang, and Xue-Min Song.
• Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Wuchang, Hubei Province, China.
• Shock. 2018 Nov 1; 50 (5): 606-612.

ObjectiveNucleotide-binding oligomerization domain 2 (NOD2) is the innate receptor of muramyl dipeptide (MDP). Our previous study revealed that MDP could enhance thermal injury-induced inflammatory cytokine production and organ function injury in rats. The present study was to determine the effect of MDP on autophagy and NOD2/receptor-interacting serine/threonine protein kinases (RICK) signaling pathway of lung injury after thermal injury.MethodsForty male Sprague-Dawlay rats were randomly divided into four groups: normal control (NC) group, MDP group, Scald group, and MDP + Scald group. Scald group only suffered 20% total body surface area third-degree (TBSA) thermal injury. MDP group was only administered 5.0 mg/kg MDP through the left femoral vein; 5.0 mg/kg MDP was administered through the left femoral vein at 24 h after thermal injury in the MDP + Scald group.ResultsTBSA thermal injury (20%) not only significantly increased the plasma inflammatory cytokines production, but also elevated the expression of LC3-I/II, the accumulation of autophagosome in the lung tissue. Compared with the Scald group, MDP + Scald double hit led to more serious inflammatory responses and higher expression of NOD2 mRNA, RICK, NF-κB p65, LC3-I/II, and the accumulation of more autophagosome in the lung tissue.ConclusionsMDP enhances thermal injury-induced autophagy and proinflammatory cytokine response of lung injury, which could be achieved via activating the NOD2/RICK signaling pathway in rats.

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