22 December 2008
Researchers shed light on bacterial resistance
Colchester Campus
A breakthrough by Essex researchers has uncovered vital information about how bacteria resist attack by the human body’s immune system.
Biochemists at the University, working with colleagues from the University of Sheffield, have discovered how an enzyme mechanism helps Escherichia coli (E. coli) bacteria to resist attack.
E. coli, which causes a number of serious diseases, 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 this week by the prestigious international journal Nature Chemical Biology, Essex biochemists and Sheffield microbiologists 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 blood volume, at high doses the body’s immune system uses nitric oxide to attack invading bacteria.
The researchers discovered that the cytochrome bd enzyme was able to prevent 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.
Professor Chris Cooper, who heads the Essex team, said: ‘This is an exciting breakthrough. 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 already knew that cytochrome bd levels increased 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 a long list of serious diseases including dysentery, diarrhoea, bladder infections and kidney failure, understanding how it resists attack by the host’s immune system is an important discovery.
‘No protein resembling cytochrome bd exists in the human body. Therefore future research might be able to target cytochrome bd with specific drugs and kill invading bacteria, whilst not harming the human patient.’
ends
Notes to Editors
The complete paper as published in Nature Chemical Biology can be viewed at http://www.nature.com/nchembio/journal/vaop/ncurrent/full/nchembio.135.html
ContactsFor further information please contact the University of Essex communications office on 01206 874377 or e-mail comms@essex.ac.uk.
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