Researchers discover new ways to treat chronic infections
Public release date: 18-Dec-2009 BINGHAMTON, NY -- Researchers at Binghamton University, State University of New York, have
identified three key regulators required for the formation and development of biofilms. The
discovery could lead to new ways of treating chronic infections.
Binghamton University, and graduate student Olga Petrova published their findings of key
regulatory events required for the formation and development of Pseudomonas aeruginosa biofilms in
PLoS Pathogens, a peer-reviewed, open-access journal published online by the Public Library of
Science.
"We have found a pathway of how the formation of biofilms is controlled," Sauer said. "If we can
figure out how to make use of this newly discovered genetic program, we can interfere with
the formation of biofilms and either prevent or treat biofilm infections more successfully."
revert established biofilms to an earlier developmental stage.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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springshowers
Frequent Contributor (1K+ posts)
Member # 19863
posted
Thanks for that article.
Sounds promising and So glad that there is a grant given for further research.
We got to find ways around these biofilms.
And the fact that people are thinking of ways besides trying to always pick away at them or disolve them is inspiring.
I think we all should put together all the ways we have heard of or tried or been told to try that will address the biofilm issue.
I wonder what that list would look like...
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which says that this pathogen is a paradigm for biofilm formation. So does that mean all biofilms have these features or will it be different with different pathogens? In other words, can we extrapolate from this to borrelia?
In Alan McDonalds work, shown on an internet website, it displays a graphic whick appears to demonstrate seeding from a biofilm. Is this one reason why we keep getting symptoms returning? As seeds are produced from the biofilm?
Here is an interesting paragraph from the second article:
"...the formation of the matrix cavity and microcolony dispersion. These data provide a mechanism for how P. aeruginosa builds a matrix and subsequently a cavity to free a portion of cells for seeding dispersal. Direct visualization reveals that Psl is a key scaffolding matrix component and opens up avenues for therapeutics of biofilm-related complications."
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posted
And here are grants in Sauer's name from NIH:
Grant Number PI Name Project Title 1R01AI075257-01A209 SAUER, KARIN Role of BdlA in biofilm dispersion and virulence properties of P. aeruginosa
1R01AI080710-01A109 SAUER, KARIN Role of PA4878 in biofilm antimicrobial resistance
2R15HL073835-02 SAUER, KARIN P. aeruginosa biofilm specific proteins and regulators
More info on these grants is available at the CRISP website (NIH grants database).
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Pinelady
Frequent Contributor (5K+ posts)
Member # 18524
posted
This group just received a 5 year grant to study the effects of olive oil in breast cancer prevention. So they must have some biological proof it does something. Spring I would like to see that list too. LOL
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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posted
I don't really understand where biofilms grow. If this is being tested in blood samples, how does it grow in a moving environment? Attached to blood vessel walls? Free floating? How is it removed by a blood sample? Does it grow in tissues too?
Puzzled at the ALS interest as they have never had the slightest inclination to pursue a bacterial causation.
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posted
Lou, some quick responses...just my opinions:
If this is being tested in blood samples, how does it grow in a moving environment?
In the ``stages'' of biofilm growth, or when the conditions are favorable, biofilm formations can break up (or break off) and flow into another part of the body where they can regerminate. These formations can involve one (monomicrobial) or many (polymicrobial) species of microbes. I've posted study abstracts on candida-MRSA joining forces biochemically to create a tougher biofilm.
Attached to blood vessel walls?
Yes, this formation is documented.
Free floating?
Yes, see above. But capturing this is like herding cats, much like finding Bb floating in the blood - it's ``catch as catch can.''
How is it removed by a blood sample?
Good question. Don't forget that blood draws from the ear lobe may provide different results from the arm; but I don't think that matters in the Fry test. Again, luck of the draw (very punny, eh?)
Does it grow in tissues too?
I believe so! Also, most microbes can create biofilms...they've been doing this for eons. They do this in nature, and as we are learning, within the human body.
-------------------- My biofilm film: www.whyamistillsick.com 2004 Mycoplasma Pneumonia 2006 Positive after 2 years of hell 2006-08 Marshall Protocol. Killed many bug species 2009 - Beating candida, doing better Lahey Clinic in Mass: what a racquet! Posts: 830 | From Mass. | Registered: Aug 2006
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Pinelady
Frequent Contributor (5K+ posts)
Member # 18524
posted
Yes. I think thats why we get the thick blood.
It could very well be caused by the biofilms, not the actual blood itself.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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