New research reveals fresh clues on the infection-fighting properties of cranberries. Researchers in Canada showed how cranberry extract rich in a particular type of compound successfully disrupted cell-to-cell communication in bacteria responsible for hard-to-treat infections.
The team - from McGill University in Montreal and INRS-Institut Armand-Frappier in Laval, both in Canada - reports the discovery in the journal Scientific Reports. Previous studies have already shown that cranberries contain proanthocyanidins (PACs), a class of compound that fends off illness through various antibacterial properties. For example, they can stop certain bacteria from sticking onto the wall of the bladder and causing a urinary tract infection.
However, the team behind the new study also wanted to find out if cranberry compounds can control the virulence of bacteria, and therefore reduce the severity of an infection. They suggest their findings not only give fresh clues on how PACs in cranberries fight bacteria, but they could also lead to new approaches to infection control.
Cranberry compounds disrupt bacterial cell communication
For their study, the team used fruit flies - a useful model for studying human infections at the level of cells and molecules. They found severity of bacterial infection was reduced in fruit flies fed on cranberry extract rich in PACs, compared with cranberry-free fruit flies. The cranberry-fed flies also lived longer.
Further investigation revealed the cranberry PACs disrupt a cell communication process called "quorum sensing" that forms an essential link in a chain of events involved in the spread and severity of chronic bacterial infections. The research focuses on a bacterium called Pseudomonas aeruginosa, which can cause infections in hospital patients and people with weak immune systems.
Patients on breathing machines, fitted with catheters, or with burns or surgical wounds are potentially at risk for serious, life-threatening infections.
Implications for antibiotic resistance
Pseudomonas infections are generally treated with antibiotics. However, because of increasing antibiotic resistance, these and other hospital-acquired bacterial infections are becoming harder to treat.
In the United States, there are an estimated 51,000 healthcare-associated P. aeruginosa infections every year. Of these, around 13 percent are multi-drug resistant, and about 400 deaths are due to these infections.
In their paper, the researchers discuss the relevance of their findings to the problem of drug resistance. They found that while the cranberry PACs disrupted bacterial quorum sensing, this did not kill the cells - it just disrupted their communication and spread.
They suggest this could be important because one reason conventional antibiotics lead to drug resistance is because they kill bacteria - which they note poses "strong selective pressure in any environment."
However, the authors also point out it would be "naive to presume" that by disrupting quorum sensing one would not be placing any selective pressures that might lead to resistance against drugs that work using this mechanism.
Nonetheless, the findings are still useful in that they "expand our strategies for combating pathogen resistance by identifying novel anti-microbial and anti-virulence agents," they conclude.
The study was funded by the Natural Sciences and Engineering Research Council of Canada, the Wisconsin Cranberry Board, and the Cranberry Institute.
Every year, millions of people are treated for cystitis, but despite its prevalence, the disease is still a scientific mystery. Now a research team from University of Southern Denmark has succeeded in identifying how the bacteria responsible for the disease cause the disease to develop. This is a cause for optimism that more effective treatment methods can be developed.
You feel the urge to urinate every two minutes, but you can only manage to squeeze out a few drops, and it stings terribly. Almost every woman has experienced cystitis, and some even experience it as a recurring annoyance.
In cases of a bacterial infection, the doctor may prescribe antibiotics. But these bacteria have a special ability to survive this treatment and cause a new infection. Now a Danish research team is reporting that they have made a discovery that potentially could lead to a new and radically different method of treatment.
Systematic monitoring of the bladder wall
The research team has developed a model that enables systematic observation and analysis of bacteria from each step in the bacteria's invasion of the bladder wall.
"Now we know important details on how the bacterium enters the phases that poses a threat. And we know how we can potentially prevent the bacteria from reaching that stage" explains head of research Jacob Møller-Jensen from the Department of Biochemistry and Molecular Biology at the University of Southern Denmark.
The research team also consists of Postdoc Surabhi Khandige, Department of Biochemistry and Molecular Biology, as well as participants from the Department of Clinical Microbiology at Odense University Hospital, led by senior researcher Thomas Emil Andersen, Department of Clinical Research.
The bacteria attach themselves to the inside of the bladder
Cystitis is usually due to special E. coli bacteria, which are able to invade cells in the urinary tract. The bacteria attach themselves to the inside of the bladder and grow. In response, the bladder rejects the outer layer of cells and thereby flushes many of the bacteria out in the urine. This produces the cloudy urine that is typical of a urinary tract infection.
However, some E. coli bacteria are cunning enough to avoid being flushed out. In a fascinating way, they alter their form and become extremely long (a process known as filamentation). This improves their ability to attach themselves to the bladder wall and thus avoid being flushed out. This in turn sets the stage for the bacteria to spread further and to take over and destroy one bladder cell after another. Finally, the bacteria reach the bottom layer of bladder cells, which they penetrate and then stop dividing. At this stage, neither antibiotics nor the body's immune system can reach the bacteria.
Become long and thin
"Scientists have long known that this bacterium is capable of some very specific tricks, including changing shape during the infection. But until now it has been difficult to discover how the bacterium manages this", explains Surabhi Khandige.
"The bacteria's ability to form long filaments is crucial to their ability to spread and thus for cystitis to develop". In order to study the bacteria's behaviour, the researchers constructed an artificial bladder model. The principle of the model is that the inside of a small chamber is lined with bladder cells, and when they have established themselves, human urine is sent into the chamber, thereby producing an artificial bladder. Then the E. coli bacteria are sent in and their activity is monitored.
"We studied the course of the infection through a microscope and we collected and studied bacteria from the various stages of the infection process. This enabled us to identify the mechanism that causes the bacteria to become filamentous. This is the first time such a detailed insight has been achieved, and it provides obvious opportunities to control this bacterium's activities and prevent the initial stage of the infection", says Jacob Møller-Jensen.
Mice did not develop cystitis
In the laboratory, the researchers tried to deactivate the mechanism that usually makes the bacteria long and thin. The ability of the bacteria to cause cystitis was then tested in mouse studies.
"Not only did we see that the bacteria were unable to cause a robust infection. We also saw that the bacterium's ability to penetrate into the deeper layers of the bladder wall declined sharply. In other words, when we deactivate the mechanism, we undermine the bacterium" says Thomas Emil Andersen, and continues:
"This offers hope that we can devise new treatment strategies to prevent problematic and recurrent urinary tract infections".
Salmonella behaves in the same way
E. coli is not the only bacterium that uses filamentation as a survival strategy. The same phenomenon can be observed, for example, in Salmonella and Klebsiella, which today are resistant to many antibiotics.
"It will be interesting to examine whether these bacteria can be controlled in the same way", says Thomas Emil Andersen.
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