Mitochondria as a cause of inflammation following injury
Cellular damage caused by mechanical trauma, hemorrhage and sepsis can release mitochondria. Thus, inflammatory forms that follow traumatic episodes seem to be due to mitochondria that when released into the blood activates polymorphonuclear neutrophils and are then attacked by the immune system because they are mistaken for bacteria. Mitochondria are, in fact, evolutionary endosymbionts deriving from bacteria and as such they may evoke bacterial molecular structures. The study is based on research of mitochondrial DNA in the blood stream. It was found that after trauma mitochondrial DNA levels can increase up to thousands of times compared to the norm. The countercheck was carried out by injecting mitochondria in the blood of test animals, which caused inflammation. Thus, signals through innate immune pathways are released identical to those activated in sepsis/sepsis-like state. The release of mitochondria as a result of cellular injury creates a fundamental link between trauma, inflammation and Systemic inflammatory response syndrome (SIRS). Therefore, it is the presence of mitochondria that activates the immune system and not a bacterial infection as has been assumed until recently.
Therefore mitochondria can be considered the core of many determining physiological and pathological processes, cellular aging through inflammaging as well as post-traumatic inflammation.