• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Attacking Biofilms That Cause Chronic Infections

Waverunner

Senior Member
Messages
1,079
Well, it's no breakthrough but this study points towards a big problem we have with bacterial infections. In many cases, bacteria form biofilms and therefore are protected from antibiotics. Antibiotics will only touch the free-flow bacteria while the biofilms remain as a constant reservoir for bacterial infection. Right now, the only working method is to remove the biofilm by surgery. This is not only very invasive in many cases, but there is also no guaranty that the biofilms and the infections will not return a few weeks later.

We have no approved drugs at the moment, which break up these biofilms but this will hopefully change fast. In this study they found out that certain proteins are used as glue or cement to build these biofilms. Concentrating on these proteins and destroying them would destroy the whole biofilm building. I don't know how long it will take, till we have these new drugs.

http://www.sciencedaily.com/releases/2012/07/120712144747.htm

ScienceDaily (July 12, 2012) — A clever new imaging technique discovered at the University of California, Berkeley, reveals a possible plan of attack for many bacterial diseases, such as cholera, lung infections in cystic fibrosis patients and even chronic sinusitis, that form biofilms that make them resistant to antibiotics.

By devising a new fluorescent labeling strategy and employing super-resolution light microscopy, the researchers were able to examine the structure of sticky plaques called bacterial biofilms that make these infections so tenacious. They also identified genetic targets for potential drugs that could break up the bacterial community and expose the bugs to the killing power of antibiotics.
"Eventually, we want to make these bugs homeless," said lead researcher Veysel Berk, a postdoctoral fellow in the Department of Physics and the California Institute for Quantitative Biosciences (QB3) at UC Berkeley.
Berk and his co-authors, including Nobel laureate and former UC Berkeley professor Steven Chu, report their findings in the July 13 issue of the journal Science.
"In their natural habitat, 99.9 percent of all bacteria live as a community and attach to surfaces as biofilms; according to the National Institutes of Health, 80 percent of all infections in humans are related to biofilms," Berk said.
The researchers were able to employ new techniques that allowed them to zoom into a street-level view of these biofilms, where they learned "how they grow from a single cell and come together to form rooms and whole buildings," Berk said. "Now, we can come up with a logical approach to discovering how to take down their building, or prevent them from forming the building itself."
Combining super-resolution microscopy with the technique Berk developed, which allows continuous labeling of growing and dividing cells in culture, biologists in many fields will be able to record stop-motion video of "how bacteria build their castles," he said.
"This work has led to new insights into the development of these complex structures and will no doubt pave the way to new approaches to fighting infectious disease and also bacteriological applications in environmental and industrial settings," said Chu, a former UC Berkeley professor of physics and of molecular and cell biology and former director of the Lawrence Berkeley National Laboratory.
Bacteria are not loners
The popular view of bacteria is that they are free-living organisms easily kept in check by antibiotics, Berk said. But scientists now realize that bacteria spend most of their lives in colonies or biofilms, even in the human body. While single bacteria may be susceptible to antibiotics, the films can be 1,000 times more resistant and most can only be removed surgically.
Implants, such as pacemakers, stents and artificial joints, occasionally become infected by bacteria that form biofilms. These biofilm sites periodically shed bacteria -- adventurers, Berk calls them -- which can ignite acute infections and fever. While antibiotics can knock out these free-swimming bacteria and temporally calm down the infection, the biofilm remains untouched.The only permanent solution is removal of the biofilm-coated device and replacement with a new sterilized implant.
A permanent bacterial biofilm in the sinuses can ignite an immune response leading to chronic sinus infections, with symptoms including fever and cold-like symptoms. So far, the most effective treatment is to surgically remove the affected tissue.
Bacteria also form permanent, mostly lifelong, biofilms in the mucus-filled lungs of cystic fibrosis patients and are responsible for the chronic lung infections that lead to early death. Although long-lasting antibiotic treatment helps, it cannot eradicate the infection completely.
To study a biofilm formed by cholera bacteria (Vibrio cholerae), Berk built his own super-resolution microscope in the basement of UC Berkeley's Stanley Hall based on a 2007 design by coauthor Xiaowei Zhuang, Chu's former post-doctoral student who is now a professor at Harvard University. To actually see these cells as they divided to form "castles," Berk devised a new technique called continuous immunostaining that allowed him to track four separate target molecules by means of four separate fluorescent dyes.
He discovered that, over a period of about six hours, a single bacterium laid down a glue to attach itself to a surface, then divided into daughter cells, making certain to cement each daughter to itself before splitting in two. The daughters continued to divide until they formed a cluster -- like a brick and mortar building -- at which point the bacteria secreted a protein that encased the cluster like the shell of a building.
The clusters are separated by microchannels that may allow nutrients in and waste out, Berk said.
"If we can find a drug to get rid of the glue protein, we can move the building as a whole. Or if we can get rid of the cement protein, we can dissolve everything and collapse the building, providing antibiotic access," Berk said. "These can be targets for site-specific, antibiotic medicines in the future."
Super-resolution microscopy: painting with light
Berk is a biologist trained in physics and optics with expertise in imaging the structures of proteins: He was part of a team that a few years ago determined the atomic-scale structures of the ribosome, the cellular machine that translates genetic message into a finished protein.
He suspected that powerful new super-resolution light microscopy could reveal the unknown structure of biofilms. Super-resolution microscopy obtains 10 times better resolution than standard light microscopy -- 20 instead of 200 nanometers -- by highlighting only part of the image at a time using photo-switchable probes and compiling thousands of images into a single snapshot. The process is much like painting with light -- shining a flashlight beam on a dark scene while leaving the camera shutter open. Each snapshot may take a few minutes to compile, but for slow cellular growth, that's quick enough to obtain a stop-action movie.
The problem was how to label the cells with fluorescent dyes to continuously monitor their growth and division. Normally, biologists attach primary antibodies to cells, then flood the cells with fluorescent dye attached to a secondary antibody that latches onto the primary. They then flush away the excess dye, shine light on the dyed cells and photograph the fluorescence.
Berk suspected that a critically balanced concentration of fluorescent stain -- low enough to prevent background, but high enough to have efficient staining -- would work just as well and eliminate the need to flush out excess dye for fear it would create a background glow.
"The classical approach is first staining, then destaining, then taking only a single snapshot," Berk said. "We found a way to do staining and keep all the fluorescent probes inside the solution while we do the imaging, so we can continuously monitor everything, starting from a single cell all the way to a mature biofilm. Instead of one snapshot, we are recording a whole movie."
"It was a very simple, cool idea, but everyone thought it was crazy," he said. "Yes, it was crazy, but it worked."
 

Waverunner

Senior Member
Messages
1,079
nanonug: I watched the whole video and it was very interesting. Phage therapy is currently only available in Georgia and I guess we still need more studies before it will be approved in the Western world. Moreover, I don't understand why it is not used for biofilms, when it is already available.

adreno: Same here, the question is, why don't hospitals and doctors use polysaccharidases or proteolytic enzymes? This study was conducted for food so it may not be applicable for humans.

Here is a new study, where the "SPLUNC1" gene seems to be a good target to thin mucus for cystic fibrosis and COPD. In my eyes it takes much too long and government puts up much too many hurdles till treatments become available.

http://www.sciencedaily.com/releases/2012/07/120713122947.htm

ScienceDaily (July 13, 2012) — University of North Carolina scientists have uncovered a new strategy that may one day help people with cystic fibrosis and chronic obstructive pulmonary disorder better clear the thick and sticky mucus that clogs their lungs and leads to life-threatening infections.

In a new report appearing online in The FASEB Journal, researchers show that the "SPLUNC1" protein and its derivative peptides may be able to help thin this thick mucus by affecting the epithelial sodium channel (ENaC). Not only does this research have implications for cystic fibrosis and COPD, but it also enhances the understanding of hypertension due to the role it also plays in controlling blood pressure.
"We hope that this study will pave the way for a new class of peptide-based channel inhibitors that can help reverse the mucus dehydration seen in Cystic Fibrosis and COPD," said Robert Tarran, Ph.D., a researcher involved in the work from the Cystic Fibrosis/Pulmonary Research and Treatment Center at the University of North Carolina in Chapel Hill. "This would help restore mucus clearance and kick-start the lung's ability to clear unwanted pathogens."
To identify which part of SPLUNC1 actually affects ENaC, scientists eliminated parts of the protein until it lost function. In fact, even after the eliminating 85 percent of SPLUNC1, it still affected ENaC, suggesting that the ENaC inhibitory domain was in the remaining 15 percent. Researchers then synthesized an 18-amino acid peptide of this region and tested its ability to bind to ENaC and to inhibit fluid absorption in human bronchial epithelial cells derived from people with and without cystic fibrosis. This peptide inhibited ENaC and fluid absorption in all systems tested, without affecting structurally-related ion channels. They also found that ENaC activity was affected for more than 24 hours in cystic fibrosis airway cultures, suggesting that this peptide may be therapeutically beneficial for the treatment of cystic fibrosis patients who suffer from over-active ENaC and consequentially have too little lung fluid.
"Breathing is something most healthy people take for granted." said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "However, people with cystic fibrosis and COPD battle for every breath because sticky mucus plugs their airways. This research should give scientists a new way of clearing the air for people with cystic fibrosis and COPD."
 

xchocoholic

Senior Member
Messages
2,947
Location
Florida
Great info once again.

I just wonder if we don't have good biofilms too tho so these treatments would
be dangerous if we broke up the wrong biofilm.

Fwiw, Guafenasin (sp ?) breaks up mucous. Would that work ?

I also just read that candida has biofilms too. So when they say that they can't break up these bacteria biofilms
with antibiotics have they tried using a candida killer at the same time ? Or guafenasin ?

I'm going to try this .. I'm doing a parasite cleanse which includes anti bacterial and anti fungus agents too. I'm going
to get some guafenasin to see how I feel. If you don't hear from me again, you'll know what happened. Lol

Tc .. X
 

August59

Daughters High School Graduation
Messages
1,617
Location
Upstate SC, USA
Lumbrokinase, Nattokinase and Serrapeptase have all been used to try and breakdown biofilms. There are a good many articles on the internet concerning biofilm treatment.
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
has anyone had any success using natto or serrapeptase with antibiotics(abx) for sinusitis??
From some recent reading it seems that many chronic sinus sufferers have bacterial biofilm infections which can the reason why abx dont work or they help but symptoms return when abx stopped.
 

FunkOdyssey

Senior Member
Messages
144
It seems implausible to me that an orally-administered enzyme will reach a biofilm on the external surfaces of the sinuses in any significant quantity. Perhaps if it were dissolved in saline and administered with nasal irrigation, assuming that was tolerated.
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
if oral abx reach the sinuses then i thought it might be possible than an oral treatment for biofilms in the sinuses is also possible???? But i just dont know?
 

adreno

PR activist
Messages
4,841
has anyone had any success using natto or serrapeptase with antibiotics(abx) for sinusitis??
From some recent reading it seems that many chronic sinus sufferers have bacterial biofilm infections which can the reason why abx dont work or they help but symptoms return when abx stopped.
Yes! High dose proteolytic enzymes has been the only thing to help me get rid of sinusitis. I haven't taken abx though, I believe you don't need that.
 

adreno

PR activist
Messages
4,841
I swallow them. They go in the bloodstream. Before taking them I had mucous so hard I couldn't cough it up, and my nasal passages were blocked. After taking (lots) of enzymes my mucous got thin and runny, and once the nasal passages were clear, the sinusitis cleared up on it's own. I was taking 4 x the recommended dose of enzymes. Now I just take the normal dose.
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
I swallow them. They go in the bloodstream. Before taking them I had mucous so hard I couldn't cough it up, and my nasal passages were blocked. After taking (lots) of enzymes my mucous got thin and runny, and once the nasal passages were clear, the sinusitis cleared up on it's own. I was taking 4 x the recommended dose of enzymes. Now I just take the normal dose.

Was it Serrapeptase u took ??
 

end

Messages
263
I took a combo of "Medizym" (same as wobenzyme), "Serrazimes" (mushroom-based analogue of serrapeptase), and "Mucostop" (Enzymedica). Serrapetase gives me lung problems.

Kirkland also has a potentially interesting product called "Biofilm defense".

Biofilm Defense(KirkMan Labs) was formulated by Dr Usman.. one of the leaders in GI Biofilms/protocols.

Adreno how much exactley did you take of the three above products?

I'm finding 1x 3cap per day of the combination(above) enzyme product is starting to give me stomach cramps in the mornings
 

Creekee

Senior Member
Messages
143
Location
Arizona
@xchocolholic,

Interesting thought re guifenasin. Somewhere there's a study showing it helps CFS. Wouldn't that be fascinating if it was because it busts biofilm?

Also, re florescent imaging: I think that's how Stephen Fry is photographing his protomyxzoa. It's a proprietary process and you get a micro photo of the bug.

Fascinating!