Scientists at Singapore's Institute of Molecular and Cell Biology (IMCB), under the Agency for Science, Technology and Research (A*STAR), have identified the protein, WIP1, as the molecular "brake" that curbs severe inflammation in the body.
The findings may prove relevant to developing more effective treatments against sepsis, the severe inflammatory condition caused by bacterial infection that afflicts many patients in intensive care units (ICU).
In their paper, "WIP1 phosphatase is a negative regulator of NFκB signaling," published in the May 2009 issue of Nature Cell Biology (NCB), the IMCB scientists described their results showing the importance of WIP1 as an effective suppressor of inflammation and explained how the body was able to cope with an excess of inflammation brought on by the hyperactivation of the NFκB protein complex, is a signaling molecule that plays a key role in triggering inflammation.
"We have shown that WIP1 plays a critical role in suppressing the activity of NFκB and keeping NFκB levels within a safe range," said IMCB principal investigator Vinay Tergaonkar, Ph.D., who headed the research team. "In doing so, WIP1 minimizes the extent of inflammatory response that could lead to septic shock and subsequent death of patients."
Dr. Tergaonkar and his colleagues compared the inflammatory response in mice lacking in WIP1 and in a control group of mice with normal WIP1 levels. The inflammatory response was higher in the WIP1 deficient animals. Correspondingly, the inflammatory response in mice with high WIP1 levels was suppressed.
In separate research, a second group of scientists led by Dr. Tergaonkar found further evidence linking chronic inflammation to the development of cancers such as that of the stomach and liver.
Dr. Tergaonkar and his colleagues discovered that the kinase enzyme IκB kinase 2 (IKK2), which is known for causing in
|Contact: Cathy Yarbrough|
Agency for Science, Technology and Research (A*STAR), Singapore