Intermedin protects against sepsis by concurrently re-establishing the endothelial barrier and alleviating inflammatory responses

Fei Xiao, Denian Wang, Lingmiao Kong, Min Li, Zhongxue Feng, Bingxing Shuai, Lijun Wang, Yong’gang Wei, Hongyu Li, Sisi Wu, Chun Tan, Huan Zhao, Xuejiao Hu, Jin Liu, Yan Kang, Xuelian Liao, Yan Zhou and Wei Zhang ()
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Fei Xiao: Sichuan University
Denian Wang: Sichuan University
Lingmiao Kong: Sichuan University
Min Li: Sichuan University
Zhongxue Feng: Sichuan University
Bingxing Shuai: Sichuan University
Lijun Wang: Sichuan University
Yong’gang Wei: Sichuan University
Hongyu Li: Sichuan University
Sisi Wu: Sichuan University
Chun Tan: Sichuan University
Huan Zhao: Sichuan University
Xuejiao Hu: Sichuan University
Jin Liu: Sichuan University
Yan Kang: Sichuan University
Xuelian Liao: Sichuan University
Yan Zhou: Sichuan University
Wei Zhang: Sichuan University

Nature Communications, 2018, vol. 9, issue 1, 1-15

Abstract: Abstract Sepsis is a life-threatening condition caused by dysregulated host responses to infection. Widespread vascular hyperpermeability and a “cytokine storm” are two pathophysiological hallmarks of sepsis. Here, we show that intermedin (IMD), a member of the calcitonin family, alleviates organ injury and decreases mortality in septic mice by concurrently alleviating vascular leakage and inflammatory responses. IMD promotes the relocation of vascular endothelial cadherin through a Rab11-dependent pathway to dynamically repair the disrupted endothelial junction. Additionally, IMD decreases inflammatory responses by reducing macrophage infiltration via downregulating CCR2 expression. IMD peptide administration ameliorates organ injuries and significantly improves the survival of septic mice, and the experimental results correlate with the clinical data. Patients with high IMD levels exhibit a lower risk of shock, lower severity scores, and greatly improved survival outcomes than those with low IMD levels. Based on our data, IMD may be an important self-protective factor in response to sepsis.

Date: 2018
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DOI: 10.1038/s41467-018-05062-2

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