"A surprising new theory developed at the University of Nebraska Medical Center (UNMC) in Omaha, Nebraska, suggests that some bacterial cells act as ``suicide bombers'' in cell communities,
with the altruistic intention of dying for the common good - and in the process, strengthening other cells that then become resistant to antibiotic drugs.
The finding could aid future research into developing drugs that can skirt the potentially catastrophic problem of bacterial resistance to antibiotics.
In a paper published April 23 in Proceedings of the National Academy of Science, Kenneth Bayles, Ph.D., of UNMC, writes that ``programmed cell death'' in bacterial communities is a form of altruism that benefits the larger community of cells and helps strengthen them.
``People get caught up in the idea that altruism is a behavior that requires deep thought, planning, and feelings such as caring,'' Bayles said. But he argues through his research that altruism appears to be an innate function in cell death, or ``lysis.''
Three years ago, Dr. Bayles, a professor of pathology and microbiology at UNMC, began growing cells in biofilm to observe how communication between cells - known as ``quorum sensing'' - affects their survival.
He observed that when cells are forming a biofilm - a colony of bacteria that contains resistant organisms and is involved in many antibiotic-resistant infections - they perform a function that enables them to leave a unique imprint on the world: their DNA.
A small percentage of cells explode in a process called ``lysis,'' leaving behind a sticky residue that contains DNA and other cellular bioproducts which are then incorporated into the larger cell community to build a stronger biofilm.
``For a long time, microbiologists viewed bacteria as wholly simplistic organisms that lived alone and died alone,'' said Dr. Bayles, noting that the discovery of ``quorum sensing'' nearly 40 years ago was a giant leap forward in understanding the complexity of communication and interaction between cells.
``My research takes the concept to the extreme, with the idea that a fraction of the bacterial population actually dies for the good of the community.''
Dr. Bayles' hypothesis could represent a paradigm shift in one of the cornerstones of microbiology, because understanding how cells die naturally - or how they commit ``suicide'' - could yield entirely new ways of killing them clinically. Previously, programmed cell death has been observed only in higher species.
He compares the process to what happens in a colony of honeybees or ants, which share 75 percent of their DNA. If something endangers one of them, a few others react altruistically - stinging intruders to defend the colony. ``Sting once, and you're dead,
but it's for the good of the colony,'' Dr. Bayles said. Because bacteria in a biofilm share 100 percent of their DNA, their ``suicide mission'' is more pronounced; instead of just a few cells dying, many die and leave behind their DNA, thus strengthening the survivors
Researchers have struggled with the question of why biofilms are extremely resistant to antibiotic drugs.
``We don't know why, but we think it's because the cell death function is suppressed in the cells that don't commit suicide, making them tolerant to antibiotics,'' Dr. Bayles said.
``In biofilm infections, if we can turn the cell death function back on, we can make them less resistant to antibiotics. Our research uncovers new targets for antibiotics, which we desperately need.''
Programmed cell death in mammals is a major topic in cancer research, and Bayles said his findings could potentially aid researchers trying to develop cancer drugs.
Bayles' findings are bound to be controversial, because he assigns a highly intellectual characteristic to these bacterial cells, although he says this altruistic behavior is likely an innate function.
``This has been brewing for the past 15 years, but now we've made this leap and we can say we've seen programmed cell death in biofilm,'' Dr. Bayles said.
``Some microbiologists have been slow to accept that programmed cell death makes sense in bacteria because they are single-celled, but many are now coming around to the idea.''
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kelmo
Frequent Contributor (1K+ posts)
Member # 8797
posted
Little ObiWanKenobi's? "Strike me down, Vader, and I'll become more powerful than you can imagine".
Biofilm seems to be more important a factor in this bacteria survival. I know that one idea is to have one antibiotic that punches wholes in the biofilm, and one to kill the bacteria.
Then, what do we do with that stray DNA? How do we bind it and send it OUT?
This is quite an interesting find, Micul, and I'll share it with my microbiologist doc.
Has Dr F said anything to you about not taking other metal minerals besides Magnesium like Chromium/Vanadium/Selenium ? Does he think that calcium is ok?
Breaking the biofilm barrier: Will it help us conquer infectious disease?
From Contemporary Urology, September 2001 Bacteria are ubiquitous in our environment. The vast majority of bacteria do not live in a free-swimming planktonic form, but rather in the self-produced, protective environment of a biofilm,
which seems to explain why some infections are nearly impossible to eradicate. Spend a weekend unclogging bathroom pipes or slipping on the rocks in a mountain stream and you will understand some of the other ways biofilms affect us.
The concept of biofilms is relatively new -William Costeiton coined the term in 1978. His early studies demonstrated the protective mechanisms of biofilms in providing an environment for bacteria away from white cells, antibacterials, and environmental stresses.
His microscopic examination of biofilms identified bacterial colonies interwoven with a polysaccharide matrix -a previously unappreciated fact. Small channels in the biofilm matrix permit the flow of oxygen, nutrients, and waste necessary to maintain microbial activity and reproduction.
While we have effective antibiotics to kill planktonic bacteria, the reservoir of bacteria contained in biofilms does not respond well to current antibiotics because of the protective nature of these structures.
The large clusters of bacteria that make up a biofilm are similar to chemotherapy-resistant malignant cells, in that organisms in the clusters' center are protected from antibacterial invasion by a "wall" of fellow bacteria.
Additional research has pointed to biofilm as producing a slower bacterial metabolism, antibiotic-degrading enzymes, and even the ability to "pump" antibacterial agents out of the biofilm before they can have any effect on the bacteria.
Indeed, bacteria in a biofilm environment can be up to 1,000 times more resistant to antibiotics than the same bacteria circulating in a planktonic state
Uropathogens and other bacteria produce biofilms unique to their species. In the lung, for example, Pveudomonas aeruginosa use their flagella to attach to each other and to the organ surface, thereby initiating colony formation.
Staphylococcus, a major biofilm-forming organism (see the photo), produces infections in wounds and on prosthetic devices such as penile prostheses and artificial urinary sphincters, and may also be involved in the initiation of catheter-borne infections.
Each year, biofilm-related infections on catheters, prosthetic devices, urinary catheters and tubes, and contact lenses cost the medical industry billions of dollars.
The Centers For Disease Control estimate that more than 65% of hospital-acquired infections have biofilms as an integral part of their morbidity and potential mortality.
Prosthetic implant infections are an excellent ease in point. Even when antibiotic agents are used in high doses and are in direct contact with the prosthetic device, these difficult, high-morbidity infections are rarely eradicated, necessitating removal of the device and its accompanying bacteria-filled biofilm.
The search for new antibiotic agents is admirable. However, the key to conquering complex urologic infections may lie instead in overcoming the bacteriaprotecting barrier effect of biofilm.
Research on antibiofilm compounds is underway at a number of laboratories across the country, and in vitro models are now available to identify the structure, architecture, unique characteristics, and production of biofilm. Despite these efforts, solutions remain elusive.
Perhaps the next generation of antimicrobials will include methods of targeting the specific genes and regulatory mechanisms in bacteria that allow them to produce biofilms.
A combination of biofilm-emulsifying drugs and good antibiotics will help us take giant steps forward in our treatment of urologic infections. *McCarthy M. Breaking up the bacterial happy home. Lancet. 2001;357(9273):2032
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