1. Academic Validation
  2. MOTS-c peptide increases survival and decreases bacterial load in mice infected with MRSA

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

  • Mol Immunol. 2017 Dec;92:151-160. doi: 10.1016/j.molimm.2017.10.017.
Dongsheng Zhai 1 Zichen Ye 1 Yinghao Jiang 1 Chengming Xu 1 Banjun Ruan 1 Yuan Yang 1 Xiaoying Lei 1 An Xiang 1 Huanyu Lu 2 Zheng Zhu 3 Zhao Yan 4 Di Wei 3 Qingyang Li 1 Li Wang 5 Zifan Lu 6
Affiliations

Affiliations

  • 1 State Key Laboratory of Cancer Biology, Department of Pharmacogenomics, Fourth Military Medical University, Xi'an 710032, PR China.
  • 2 Department of Occupational and Environmental Health and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an710032, PR China.
  • 3 Institute of Urinary Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, PR China.
  • 4 Institute of Orthopedic Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, PR China.
  • 5 State Key Laboratory of Cancer Biology, Department of Pharmacogenomics, Fourth Military Medical University, Xi'an 710032, PR China. Electronic address: [email protected].
  • 6 State Key Laboratory of Cancer Biology, Department of Pharmacogenomics, Fourth Military Medical University, Xi'an 710032, PR China. Electronic address: [email protected].
Abstract

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.

Keywords

Ahr; MAPK; MOTS-c; MRSA; Macrophage; STAT3.

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