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Release: Nov. 23, 1999

UI research helping answer questions about cystic fibrosis

IOWA CITY, Iowa -- Many times successfully attacking a problem first requires that the attackers devise a battle plan. The individuals must figure out how the other side operates and then how those operations might be dismantled. That is exactly the approach a team of University of Iowa Health Care researchers is taking with respect to bacteria that cause chronic and serious lung infections in people with cystic fibrosis.

Results from the continuing UI efforts to understand how the bacteria Pseudomonas aeruginosa (P. aeruginosa) lead to infection are being published in the Nov. 23 issue of the Proceedings of the National Academy of Sciences (PNAS).

"This is a logical extension of what has been going on about how and why that infection is so persistent," said E. Peter Greenberg, Ph.D., UI professor of microbiology and the study's lead investigator.

The PNAS article deals with quorum sensing -- a communication device involving chemical signals that bacteria rely on to cause infection. When a bacteria population reaches a certain density, quorum-sensing signals tell the community of bacteria, known as a biofilm, to activate certain genes that allow the bacteria to cause infection and disease.

The UI investigators wanted to identify the genes expressed through the quorum-sensing process. Although there had been some research into the area, the number and types of genes controlled by quorum sensing had not been studied systemically. The UI team was able to look at the entire gene make-up of P. aeruginosa thanks to the just-completed work of University of Washington researchers, who have sequenced all of the bacteria's genes.

Through their work, the UI investigators screened most of P. aeruginosa's 7,000 genes. Of those, the researchers identified 39 genes strongly regulated by quorum sensing.

"The most important thing from this work is that it begins to map out a network of what is regulated by quorum sensing that is so important to infection," Greenberg said. "More and more evidence is accumulating that suggests if we can block quorum sensing, we can incapacitate pseudomonas."

Greenberg and his co-workers, graduate student Marvin Whiteley and technician Kimberly Less, added that although this investigation revealed some interesting features of gene expression by quorum sensing, it clearly raises more questions than it answers.

Now that the UI investigators are beginning to understand quorum sensing in P. aeruginosa at the gene level, it is feasible to address these questions. The UI team is currently collaborating with researchers at the University of Washington to study which genes play a role in causing infections in animal models. In a separate, but related effort, Greenberg's lab is also working with former UI post-doctoral fellow Matt Parsek, now at Northwestern University, to ask which of the genes are required for biofilm maturation.

The research detailed in the PNAS article was supported by grants from the National Science Foundation (NSF) and the National Institutes of Health. Whiteley is supported by a NSF Research Training Grant.

University of Iowa Health Care describes the partnership between the UI College of Medicine and the UI Hospitals and Clinics and the patient care, medical education and research programs and services they provide.