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    Default Mitochondria and the Immune Inflammatory Response

    Just ran across an interesting article...Mitochondria, DAMPS, PAMPS | Learn Science at Scitable.

    Summary:
    "Mitochondria are not only the "powerhouses" of our cells, they also play a significant role in triggering severe illnesses. Zhang and his colleagues provided evidence indicating that mitochondria are the missing link to explain the observed similarities between SIRS and sepsis. Severe trauma releases mitochondrial DAMPs into the blood where they are recognized by innate immunity through PRRs and FPR1, which also sense bacteria. Because mitochondrial DAMPs have evolutionarily conserved similarities to bacterial PAMPs, the release of mitochondrial DAMPs results in a "sepsis-like" state. This new model provides clues to better understand how the systemic inflammatory response develops. What scientists still do not know is if both SIRS and sepsis can be alleviated or prevented by inhibiting these pathways with pharmaceutical compounds. More research will be needed to answer these questions."
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    Quote Originally Posted by Infinite1 View Post
    Just ran across an interesting article...Mitochondria, DAMPS, PAMPS | Learn Science at Scitable.

    Summary:
    "Mitochondria are not only the "powerhouses" of our cells, they also play a significant role in triggering severe illnesses. Zhang and his colleagues provided evidence indicating that mitochondria are the missing link to explain the observed similarities between SIRS and sepsis. Severe trauma releases mitochondrial DAMPs into the blood where they are recognized by innate immunity through PRRs and FPR1, which also sense bacteria. Because mitochondrial DAMPs have evolutionarily conserved similarities to bacterial PAMPs, the release of mitochondrial DAMPs results in a "sepsis-like" state. This new model provides clues to better understand how the systemic inflammatory response develops. What scientists still do not know is if both SIRS and sepsis can be alleviated or prevented by inhibiting these pathways with pharmaceutical compounds. More research will be needed to answer these questions."
    This is indeed interesting. Why would this be? Extracellular (mitochondrial) ATP is also detected and is an extremely potent proinflammatory signal. Mitochondria are derived from alphaproteobacteria which, being extremely energetic oxygen breathing bacteria can produce and export ATP as part of their respitory metabolism. In essence, these bacteria produce too much energy and have to get rid of it, like the return of conducting wire, via the phosphorylation of molecules. Since these bacteria are usually small, they were subject to grazing and phagocytosis by large ameboid eukaryotic cells, which obligingly returned spent phoshate carriers back. This is how mitochondria came to be. As the presence of these bacteria suggests intracellular problems, and when subsequently a cell dies, it releases them, they are a signal of infection, and a potentially lethal one. Rickettsia is a parasytic ancient relative of mitochondria. I recall reading that a coinfection with a common virus (I think if memory serves me an influenza) and a rickettsial infection was 100% fatal, whereas it is quite unusual alone.

    The release of mitochondria by an explosive collapse of a cell following an intracellular infection, due to bacterial or viral load, is common, and this scenario is dangerous as normally, mitochondria trigger a safer form of cell death when the cell is infected or no longer viable, that degrades the cell components or triggers phagocytes to do this. As such, mitochondrial release outside the cytoplasm is a sign of a serious problem. Within the body mitochondria are normally trafficked between cells within pockets of cellular cytoplasm. So mitochondria outside of such environment means something has been catastrophic. Mitochondria release many compounds that can be recognised, since cell function is generally controlled by mitochondria, including influencing the ATP and adenosine ratios.

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