Lab work discovers bladder cell secret against urinary infection
Escherichia coli bacteria behind most urinary tract
infections (UTIs) involves physically ejecting those that have
invaded host cells and escaped acid destruction.
The laboratory discovery, published in Cell, a journal for
fundamental biology research, suggests an avenue of scientific
investigation into ways of capitalizing on this natural tendency,
to help treat recurring UTIs.
Senior author Soman Abraham, PhD, from the Duke University
School of Medicine in Durham, NC, explains:
"Because E. coli are able to hide inside of the bladder cells,
it's especially difficult to treat UTIs with regular antibiotics.
"So there is increased need to find new strategies for
treatment, including co-opting any preexisting cellular tactics to
combating infection."
The professor in Duke's departments of pathology, immunology,
and microbiology and molecular genetics is also professor in the
emerging infectious diseases program at the Duke-National
University of Singapore. He suggests the financial importance
of work against urinary tract infections:
"The cost for managing UTIs in the US is close to $3 billion
annually."
Urinary tract infections - the vast majority of which are
caused by E. coli - come near the top of the list for our
most common types of infection, according to information from
the National Institutes of Health .
Because of their anatomy , which allows easier access for the
bacteria to reach the bladder, women are more prone to UTIs
than men, but around 8.1 million visits to health care providers
each year are blamed on these infections overall.
Acid envelopes that failed to degrade bacteria were
simply ejected
The basic strategy identified by the biologists was for bladder
cells to hit the ejector button on those acid envelopes that the
bacteria had successfully survived.
The first tactic called on against E. coli by bladder cells is
the normal first line of cellular defense - autophagy - or
eliminating pathogens that have entered the cell by encasing
them and shuttling them off to lysosomes.
The acidic environment of lysosomes - "capsular cauldrons," as
the Duke researchers call them - destroys pathogens. But on
entering the lysosome, some pathogens have the capacity to
neutralize the acidic environment.
The authors discovered, however, that host cells are able to
sense when lysosomes have been affected in this way, and
trigger ejection of the lysosome contents and bacteria - but
with the pathogens seemingly encased in a cell membrane,
"presumably" ensuring their elimination in urine and avoiding any
bacterial reattachment to the bladder wall.
The findings of the study come from laboratory work with
mouse models of UTIs and human bladder cells used in culture.
First author Yuxuan Miao, a doctoral candidate in Duke's
department of molecular genetics and microbiology, says:
The hope of the researchers is that the new biology will help
in identifying chemical targets to accelerate and amplify the
bladder cells' own bacterial expulsion tactics.
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