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Pure Mitochondrial DNA Does Not Activate Human Neutrophils in vitro

A. S. Prikhodko1, A. K. Shabanov2, L. A. Zinovkina1, E. N. Popova3, M. A. Aznauryan1, N. O. Lanina1, M. V. Vitushkina4, and R. A. Zinovkin3,4*

1Faculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, 119991 Moscow, Russia

2Sklifosovsky Research Institute of Emergency Care, 129010 Moscow, Russia

3Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia

4Faculty of Biology, Lomonosov Moscow State University, 119234 Moscow, Russia; fax: +7 (495) 939-0338; E-mail: roman.zinovkin@gmail.com

* To whom correspondence should be addressed.

Received December 22, 2014; Revision received January 22, 2015
Excessive activation of the innate immune system often leads to fatal consequences and can be considered as one of the phenoptotic events. After traumatic injury, various components of mitochondria are released into the circulation and stimulate myeloid cells of the innate immunity. Presumably, mitochondrial DNA (mtDNA) might activate immune cells (Zhang, Q., et al. (2010) Nature, 464, 104-107). In the present study, we investigated the role of mtDNA as a direct activator of human neutrophils, as well as a prognostic marker in patients with severe trauma. Quantitative determination of mtDNA in the plasma of these patients revealed its significant increase (p < 0.02) in the group of survivors compared to non-survivors. Highly purified mtDNA was not able to induce activation of human neutrophils, thus possibly indicating the existence of additional factor(s) ensuring the recognition of mtDNA as a damage-associated molecular pattern.
KEY WORDS: trauma, extracellular DNA, mitochondrial DNA, neutrophil activation, damage-associated molecular patterns (DAMPs)

DOI: 10.1134/S0006297915050168