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Home > Healthcare Professionals > Research Awards > Researcher Profiles > Dr. Johannes Kluwe

Dr. Johannes Kluwe, MD

Charles Trey, MD Memorial Postdoctoral Research Fellowship. Columbia University Medical Center, New York, New York. "Role of NK-kB in the Crosstalk Between Kupffer Cells and Hepatic Stellate Cells."


Dr. Johannes Kluwe, MD

Chronic liver diseases like viral hepatitis, metabolic and autoimmune disorders involve inflammation of the liver tissue and lead to the development of liver fibrosis, the replacement of healthy liver tissue with nonfunctional scar tissue. Progressive fibrosis occurs in a large proportion of patients and accounts for the development of the typical, potentially fatal complications of chronic liver disease. Currently, the only way to treat liver fibrosis is to treat the underlying disease. However, in many patients the underlying disease cannot be cured. The main objective of this study is to clarify mechanisms that promote the development of liver fibrosis. By studying two kinds of liver cells that are known to contribute to inflammation and scar formation, Dr. Kluwe hopes to find mechanisms by which inflammation contributes to scar formation and to provide a direction for the future development of treatments that specifically target and control fibrosis.

Kupffer cells are known to regulate inflammation in the liver but have no ability to produce scar tissue while hepatic stellate cells are a major source of scar tissue. Depletion of Kupffer cells almost completely prevents liver fibrosis, suggesting that Kupffer cells must provide some signal to stellate cells to promote scarring of the liver. Our preliminary data strongly suggests that Kupffer cells secrete inflammatory mediators to promote scar tissue formation by hepatic stellate cells. If interaction between Kupffer cells and hepatic stellate cells can be fully described, then it may be possible to block this signal and keep hepatic stellate cells from producing scar tissue while allowing Kupffer cells to retain their normal inflammatory function. We will attempt to identify the mechanisms by which they promote scarring by culturing these two cell types together and measuring effects of blocking candidate inflammatory molecules. We then hope to further characterize this cell-to-cell interaction in mouse models.

Page updated: August 1st, 2008