Research Papers: Pathology:
The involvement of endoplasmic reticulum stress response in immune dysfunction of dendritic cells after severe thermal injury in mice
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Xiao-Mei Zhu1,2, Ning Dong2, Yan-Bo Wang2, Qing-Hong Zhang2, Yan Yu2, Yong-Ming Yao2 and Hua-Ping Liang1
1 State Key Laboratory of Trauma, Burns and Combined Injury, Research Institute of Surgery, Daping Hospital, The Third Military Medical University, Chongqing, China
2 Department of Microbiology and Immunology, Trauma Research Center, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing, China
Yong-Ming Yao, email:
Hua-Ping Liang, email:
Keywords: endoplasmic reticulum stress; dendritic cell; immune dysfunction; burns; sepsis; Pathology Section
Received: April 18, 2016 Accepted: January 10, 2017 Published: January 19, 2017
Suppressed adaptive immune function is one of the major concerns responsible for the development of opportunistic infections and subsequent sepsis with high mortality in severe burns. Endoplasmic reticulum stress (ERS) is the endogenous self-protective mechanism, and it plays an important role in almost every process of living by regulating the balance between homeostasis and apoptosis. The current study investigated the involvement of ERS in the pathogenesis of dysfunction of dendritic cells (DCs) in burn mice. Our results show a significant ERS response in splenic DC after burn injury. Treatment with salubrinal (Sal, reported to protect cells against ERS-induced apoptosis.) decrease the apoptotic rate of DC induced by burns, and promote maturation and activation of DC, as well as the ability to promote T cell proliferation and polarization towards Th1 immunity (all P<0.05). Gene silence of XBP-1 (key molecular in ERS response) results in the increased apoptosis and suppressed phenotypical maturation of splenic DC in burn mice. These results show that the excessive ERS is essential for immunosuppression during severe thermal injury. XBP-1 plays a pivotal role in DC functional immunomodulation in burn mice. Inhibition of apoptotic ERS response benefits mice from major burns.
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