Apr. 1, 2007 In a study appearing in the April 2007 issue of The FASEB Journal, scientists from Harvard University and the University of Pittsburgh have shown for the first time that the anti-inflammatory effects of carbon monoxide originate within cells' own molecular engines, mitochondria.
Specifically, mitochondria react to low levels of carbon monoxide by releasing chemical signals that reduce or shut down the body's inflammatory response, raising the possibility for the development of new anti-inflammatory therapies, one of which may be low levels of inhaled carbon monoxide.
According to the study's first author, Brian S. Zuckerbraun, M.D. of the University of Pittsburgh, "this study may contribute to our understanding and development of controlled carbon monoxide as a therapeutic agent."
Inflammation is a normal defense mechanism used by the body to ward off infection, but over time, severe or chronic inflammation can damage tissues. In some cases, such as in organ transplantation, the body's inflammatory response over the short-term also can cause more harm than good. Current approaches to controlling inflammation are not always successful, making the need for new approaches urgent. In particular, inhaled medical grade carbon monoxide has been shown to be useful in animal models for organ transplantation, vascular injury, inflammatory bowel disease, organ injury resulting from severe blood loss, as well as experimental hepatitis and experimental pulmonary hypertension.
"The findings described in this study are particularly relevant, given that April is National Donate Life Month," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Transplants are rejected because of inflammation gone awry. If we block inflammation, as with carbon monoxide or agents that release it in a controlled fashion, we can not only make transplantation safer, but extend its benefits to many more who need it."
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