Circulating mitochondrial DAMPs cause inflammatory responses to injury

Qin Zhang, Mustafa Raoof, Yu Chen, Yuka Sumi, Tolga Sursal, Wolfgang Junger, Karim Brohi, Kiyoshi Itagaki and Carl J. Hauser ()
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Qin Zhang: Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Mustafa Raoof: Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Yu Chen: Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Yuka Sumi: Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Tolga Sursal: Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Wolfgang Junger: Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Karim Brohi: Trauma Clinical Academic Unit, Barts and the London School of Medicine & Dentistry, Queen Mary, University of London, Whitechapel Road, London E1 1BB, UK
Kiyoshi Itagaki: Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Carl J. Hauser: Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA

Nature, 2010, vol. 464, issue 7285, 104-107

Abstract: Mitochondrial revolt Mitochondria are endosymbiotic descendents of bacteria, well tolerated by the eukaryotic cells that they now serve after millions of years of co-evolution. But in extremis it seems strains in the relationship may emerge. Tests on plasma samples from patients who had suffered severe trauma show that mitochondrial DAMPs (or damage-associated molecular patterns) are released into the circulation as a result of tissue damage, where they activate neutrophils via specific formyl peptide receptors. This triggers systemic inflammation, tissue damage and apparent sepsis. These DAMPs interact with receptors that are part of the innate immune response to molecules known as PAMPs (pathogen associated molecular patterns), which are expressed on invading microorganisms, causing bacterial sepsis. This finding appears to explain the apparent sepsis sometimes associated with severe trauma even when no infection is present.

Date: 2010
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DOI: 10.1038/nature08780

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