LPS may control UTI bugs' pathogenicity, study shows

May 22, 2012

Researchers teasing out the relationship between urinary tract infection and its symptoms are zeroing in on the major component of Escherichia coli's cell wall, lipopolysaccharide (LPS), as the culprit.

Researchers teasing out the relationship between urinary tract infection and its symptoms are zeroing in on the major component of Escherichia coli’s cell wall, lipopolysaccharide (LPS), as the culprit.

Kylie Mansfield, PhD, of the University of Wollongong, New South Wales, Australia, and her colleagues showed that one serotype of LPS may prompt ATP release from the urothelium when it is stretched, whereas another serotype does not in a study she presented here yesterday.

That might spell the difference between feeling urgency with an infection or not being aware of the UTI at all because ATP is known to modulate contractility, session co-chair David Klumpp, PhD, from Northwestern University, Chicago, told Urology Times. He and his colleagues have also focused on E. coli LPS, showing that it can modulate the pain response to a UTI.

Dr. Mansfield and her colleagues treated urothelial cells with two different serotypes of LPS for 24 hours (serotypes 0111:B4 and 055:B5) and subjected them, as well as control cells, to stretch with a hypotonic Krebs solution, simulating bladder filling. With stretch, ATP release in untreated cells quadrupled, and release from cells treated with the 0111 LPS more than doubled, but cells treated with the 055 LPS did not increase ATP release.

Session co-chair Anthony Schaeffer, MD, also from Northwestern University, asked why bacteria with this LPS would "want" to do this. "It could be that by inhibiting the ATP release, it’s inhibiting voiding contractions and getting to stay around longer, so it may be that bug’s pathogenic mechanism," Dr. Mansfield speculated.

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