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Biology Articles » Biochemistry » Receptor May Increase Risk Of Urinary Tract Infections

Receptor May Increase Risk Of Urinary Tract Infections

A newly discovered chemical compound on the surface of some women's kidney cells may explain susceptibility to urinary tract infections, according to current research in the journal Biochemistry. The structure, a specific type of compound known as a glycosphingolipid, is suspected to be on urogenital tract cells in about 30% of all men and women and binds strongly to E. coli bacteria.

The research is outlined in the Nov. 21 web edition of Biochemistry, a peer-reviewed journal of the American Chemical Society, the world's largest scientific society. The article will appear in the journal's Dec. 15 print publication.

Previous studies have shown that women without ABO blood group antigens in their bodily secretions are more likely to have recurrent urinary tract infections. These women are missing the biochemical tools that put the finishing touches on a certain chemical called a glycolipid to determine blood type. "So that glycolipid becomes modified in a different way," says lead author Mark R. Stroud, Ph.D. at Northwest Hospital and the University of Washington in Seattle, "and that modification results in a compound that acts as a high affinity receptor for E. coli The big story here is that the compound itself has been identified." The compound, called sialosyl galactosyl globoside or SGG, had previously only been found in some animal cells and human cells in early stages of embryonic development.

E. coli bacteria are responsible for more than 90% of urinary tract infections, which affect an estimated 7 million women each year at a cost exceeding one billion dollars for diagnosis and treatment. Finding this bacteria-binding compound on kidney cells and the researchers have strong evidence it is on other cells lining the urogenital tract as well may provide a strategy to better treat women prone to infection, who often have to take antibiotics constantly.

Those treatment regimens "basically turn someone who is otherwise normal into having a chronic disease," says co-author and University of Washington Associate Professor of Medicine Ann E. Stapleton, M.D.. "They have to take something, often for the rest of their lives, if they want to be free of infection." Such long-term use of medicines can also create resistant strains of bacteria.

Now that scientists know the structure of SGG, "we'd like to use this as a model to create something that can then inhibit E. coli from binding," says Stroud. While cautioning that such a strategy is a long-term goal, Stapleton adds: "What we hope to do is to see whether or not competitive inhibition at the mucosal level would have some effect on prevention or, perhaps, augmentation of treatment." The researchers believe that since the bacteria wouldn't be killed just washed away mutants, and thus resistance, would not develop.

American Chemical Society. December 1998.


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