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Almost 50% patients are in intensive care units because of inflammatory complications related to illness or injury. Systemic Inflammatory Response Syndrome (SIRS) is a serious consequence of traumatic injury. The SIRS inflammatory response was long believed to result from gastrointestinal tract bacteria entering systemic circulation via the portal vein. However, research in the 1990s determined that was not the case. Now, a recent study by Carl Hauser, a trauma surgeon and immunologist at Harvard Medical School in Boston, may have revealed the cause of SIRS. Hauser and colleagues found that the plasma of traumatically injured patients contained 1,000 times more mitochondrial DNA than is found in normal plasma. Hauser hypothesized that mitochondrial debris, released from traumatically injured cells and perceived by the body as invading microorganisms, initiates an inflammatory response and the SIRS; symptoms.


Hauser and colleagues further explored this connection by injecting mitochondrial DNA into the lung tissues of experimental rats. Neutrophils migrated to the area where the mitochondrial DNA was injected and an inflammatory response resulted. When bacteria are responsible for inflammation, antibiotics are effectively used for treatment. However, in SIRS antibiotics are not always helpful. Having identified mitochondrial DNA fragments as contributing to the inflammatory response in traumatic injuries, scientists may now be able to develop a pharmacological intervention to block or slow the inflammatory response. Identification of this new mechanism that initiates inflammation may lead to effective treatment for a syndrome previously difficult to understand and to treat.


Source: Schednkman L. Deadly inflammation, but no sign of infections. ScienceNow. March 3, 2010. Available at Accessed on March 10, 2010.


Submitted by: Robin Pattillo, PhD, RN, News Editor at[email protected].