MOTS-c peptide increases survival and decreases bacterial load in mice infected with MRSA

Publication date: December 2017
Source:Molecular Immunology, Volume 92
Author(s): Dongsheng Zhai, Zichen Ye, Yinghao Jiang, Chengming Xu, Banjun Ruan, Yuan Yang, Xiaoying Lei, An Xiang, Huanyu Lu, Zheng Zhu, Zhao Yan, Di Wei, Qingyang Li, Li Wang, Zifan Lu
Sepsis is a life-threatening disease characterized by uncontrolled inflammatory responses upon pathogen infections, especially for the antibiotic-resistant strains, such as Methicillin-resistant S. aureus (MRSA). Here we demonstrated that a Mitochondria-derived peptide (MOTS-c) could significantly improve the survival rate and decrease bacteria loads in MRSA-challenged mice, accompanied with declined levels of pro-inflammatory cytokines, such as TNF-α, IL-6 and IL-1β, but with increased level of anti-inflammatory cytokine IL-10. Moreover this peptide enhanced bactericidal capacity of macrophages. Meanwhile, MOTS-c inhibited the phosphorylation mitogen-activated protein kinases (MAPK), and enhanced the expression of aryl hydrocarbon receptor (AhR) and signal transducer and activator of transcriptional 3 (STAT3) in macrophages. Overall, MOTS-c plays a beneficial role in curbing the overwhelming inflammatory bursts in the fight against MRSA infection. It may serve as a potential therapeutic agent in sepsis treatment.Highlight• MOTS-c improved survival status in mice during MRSA infection.• MOTS-c strongly enhanced bactericidal capacity of macrophages.• MOTS-c exerted an anti-inflammatory effect via suppressing MAPKs and increasing Ahr/STAT3 signaling pathways.



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