Scientists make health breakthrough
A BREAKTHROUGH by Sheffield researchers has uncovered vital information about how bacteria resist attack by the human body's immune system.
Microbiologists at The University of Sheffield, working with colleagues from The University of Essex, have discovered how an enzyme mechanism helps the E.coli bacteria to resist attack.
E.coli, which causes serious diseases like dysentery, diarrhoea, bladder infections and kidney failure, gets its energy from enzymes that react with oxygen. One of these, called cytochrome bd, is crucial for virulence - the ability of the bacteria to spread its disease.
In a study reported by the prestigious international journal Nature Chemical Biology, Sheffield and Essex researchers have used E.coli to investigate the interaction between cytochrome bd and nitric oxide gas.
Nitric oxide, the toxic by-product of car exhausts, was originally thought only to interact with mammals as an environmental pollutant. It is now known that all mammalian cells produce this gas. At low doses it is used as a signalling molecule, increasing blood flow and volume, while at high doses our immune system uses nitric oxide to attack invading bacteria.
Researchers discovered that the cytochrome bd enzyme prevents nitric oxide attack, allowing the cells to survive longer. The enzyme's resistance seemed to relate to its ability to rapidly expel the gas, allowing its replacement by the oxygen required for bacterial growth.
Prof Robert Poole, who heads the Sheffield team, said: "Our work has previously focused on mammalian enzymes that react with nitric oxide. Now we know there is a lot more to learn about the bacterial side of the equation.
"We knew cytochrome bd levels rose when we attacked bacteria with nitric oxide. This study suggests why this adaptation evolved; it could have general implications for bacterial resistance to host attack. As E.coli causes many serious diseases, understanding how it resists attack is an important discovery. No protein resembling cytochrome bd exists in humans. Therefore future research may target cytochrome bd with specific drugs and kill invading bacteria, while not harming patients."
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Wednesday 23 May 2012
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