University of Iowa News Release
March 13, 2006
Amoeba Helps UI Biomedical Researchers Study Rare Disease
The irregular "walk" of an amoeba is helping University of Iowa researchers to better understand a rare human disease that afflicts children.
According to a research highlight article in the Jan. 26 issue of the journal Nature, studies performed by University of Iowa researcher David Soll and co-workers demonstrate that the amoeba (Dictyostelium discoideum) behaves similarly to certain white blood cells and therefore is a good model for studying Shwachman-Bodian-Diamond syndrome (SBDS), a rare disease affecting the pancreas, white blood cell function and general human development. Soll and his co-workers discovered that white blood cells of SBDS patients cannot hunt down infecting bacteria, resulting in increased susceptibility to infections.
Why the amoeba is a good model for white blood cells involves a single gene, according to Soll, who serves as Emil Witschi - Roy J. and Lucille A. Carver Professor in the College of Liberal Arts and Sciences Department of Biological Sciences.
Soll and his colleagues recently identified -- in the amoeba -- the same gene that mutates in humans to cause SBDS. They engineered the SBDS gene in the amoeba so that it was fluorescent and could be localized, and they found that it traveled into the pseudopods or protruding arms that the amoebae use to crawl and hunt bacteria, just as white blood cells do to fight infection.
The findings suggest that SBDS may play a role in regulating the molecules in the cell's protruding arm, and defects in this molecule may result in a faulty hunting response, and infection.
Soll says that further studies using the model amoeba will provide information that can be transferred to humans in the treatment of this disease.
The complete research article was published in the January 2006 issue of the Journal of Cell Science. In addition to Soll, UI W.M. Keck Dynamic Image Analysis Facility researchers and study co-authors are: Deborah Wessels, Thyagarajan Srikantha, Song Yi and Spencer Kuhl, as well as L. Aravind of the National Institutes of Health.
In 2004, Soll, his colleagues and Dr. Fred Goldman, head of pediatric hematology at University of Iowa Hospitals and Clinics, discovered the behavioral basis for the SBDS defect in human white blood cells by using the 2D and 3D computer-assisted motion analysis systems pioneered in the UI's W.M. Keck Dynamic Image Analysis Facility. By studying white blood cell motility and how certain cells move in response to chemical stimuli, they found that the basic behavior of such cells from SBDS patients, called polymorphonuclear leukocytes (PMNs), is normal in the absence of a chemical stimulus. However, the SBDS cells appeared disoriented when introduced to the chemical stimulus released by bacteria that the PMNs use to hunt them down in bacterial infections. The results suggested a behavioral basis for SBDS and a single behavioral defect in white blood cells from SBDS patients. Studies of the same gene in the model soil amoeba will define the function of the SBDS gene in fighting infection, and should provide a basis for curing this defect in SBDS patients.
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