Mitochondria, Efficient Energy Production with Dangerous Side Effects?

Scientists from Harvard Teaching Medical Hospital have discovered that Mitochondria respond to trauma by creating patient inflammation and a response not unlike bacterial infection. Best known as the energy producing powerhouses of the cell (being home of the Citric Acid Cycle and oxidative phosphorylation), Mitochondria have long been recognized as ancient symbiots – not originally part of the eukaryotic cell line, but were once prokaryotes that have, through a selectively advantageous symbiotic relationship, become incorporated into the eukaryotic cell line. These organelles have their own genetic code, their own DNA, their own plasma membrane, and are able to reproduce independently of the cell. Now, this newly understood behavior may shed light onto their ancient bacterial origin.

Beth Israel scientists have shown that during respiration, molecules from spent or disrupted mitochondria escape the cell and enter the bloodstream causing an immune response with  an evolutionarily conserved similarity to bacterial infection. The study suggests that during times of severe injury when the body is undergoing rapid metabolism in response to the damage, this process is elevated and thus allows larger concentrations of the spent mitochondrial DNA to induce a cascading response in the patient. These circulating mitochondrial protein signatures ultimately cause the body to respond as though a bacterial infection were running rampant. This immune response leads to a syndrome known as Systemic Inflammatory Response Syndrome (SIRS) that can be very dangerous leading to a racing heart, fever, breathing difficulties, and eventual organ failure.

It’s interesting to think that the body contains self-destructive mechanisms like this. However problematic these by-products may be, they are definite parts of mitochondrial energy production and therefore a requirement for life as we know.

Zhang et al. Circulating mitochondrial DAMPs cause inflammatory responses to injury. Nature (2010) vol. 464 (7285) pp. 104-107.

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