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'Zinc zipper' plays key role in hospital-acquired infections

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Public release date: 4-Dec-2008

Contact: Herrell

.Herrell@...

University of Cincinnati

'Zinc zipper' plays key role in hospital-acquired infections

CINCINNATI—Hospital-acquired infections that are resistant to

traditional antibiotic treatment have become increasingly common in

recent years, confounding health care professionals and killing

thousands of Americans.

Now, in studies that could lead to new ways to prevent this growing

public health danger, a team of University of Cincinnati (UC)

researchers is exploring a " zinc zipper " that holds bacterial cells

together and plays a key role in such infections.

Hospital-acquired infections affect about 1.7 million people per year in

the United States and result in an estimated 99,000 deaths annually,

according to the Centers for Disease Control. About two-thirds of all

hospital-acquired infections can be traced to two staphylococcal

species, Staphylococcus aureus—including methicillin-resistant strains

(MRSA) that are particularly difficult to treat—and Staphylococcus

epidermidis.

In an article appearing in the Dec. 1 online edition of Proceedings of

the National Academy of Sciences, researchers in UC's department of

molecular genetics, biochemistry and microbiology detailed findings that

the presence of zinc is crucial to the formation of infection-causing

biofilms.

Staphylococci can grow as biofilms, which are specialized communities of

bacteria that are highly resistant to antibiotics and immune responses.

They are remarkably adhesive and can grow on many surfaces, including

implanted medical devices such as pacemakers, heart valve replacements

and artificial joints. Preventing or inhibiting the growth of such

biofilms would dramatically reduce the incidence of staph infections.

UC researchers in the lab of Herr, PhD, an assistant professor

and Ohio Eminent Scholar in structural biology, found that zinc causes a

protein on the bacterial surface to act like molecular Velcro, allowing

the bacterial cells in the biofilm to stick to one another. Zinc

chelation, or removal, prevented biofilm formation by Staphylococcus

epidermidis and Staphylococcus aureus. The researchers used a chelation

agent called DTPA (diethylenetriamine pentaacetic acid) to remove the

zinc from a sample biofilm.

" We've shown that if you remove the zinc, you prevent the biofilm from

forming, and if you add zinc back, the biofilm can grow, " says Herr. " So

we're hopeful that we can use this sort of approach to prevent these

biofilms from ever taking hold in the first place. "

The most practical applications, Herr says, might involve coatings for

implanted medical devices, or rinses that a surgeon could use to clear

the area around the implant.

Systemic removal of zinc, such as through an intravenous injection, is

impractical for now because DTPA is approved by the U.S. Food and Drug

Administration only for people with radio isotope poisoning. In

addition, zinc is known to activate immune cells and play many other

important roles in the body, so a proper balance would need to be developed.

###

Herr had access to funds from the Ohio Eminent Scholars Program and also

received a pilot grant from the Cincinnati Microbial Pathogenesis Center

for the study. He intends to apply for a National Institutes of Health

grant in 2009 to continue his research.

The research team, in addition to Herr, consisted of graduate student

Deborah Conrady; postdoctoral fellows Cristin Brescia, PhD, and

Katsunori Horii, PhD; and UC molecular genetics, biochemistry and

microbiology professors Alison Weiss, PhD, and Hassett, PhD.

--

ne Holden, MS, RD

" Ask the Parkinson Dietitian " http://www.parkinson.org/

" Eat well, stay well with Parkinson's disease "

" Parkinson's disease: Guidelines for Medical Nutrition Therapy "

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