 |
| Author | Post |
|---|
TikBitten
Member
| Joined: | Thu Mar 13th, 2008 |
| Location: | USA |
| Posts: | 81 |
| Status: |
Offline
|
|
Posted: Thu Dec 17th, 2009 17:06 |
|
The treatment of infectious diseases is based on compounds that traditionally aim to kill or inhibit bacterial growth, including the ABXs used in the MP. A major concern I harbor is the development of resistance to the MP antimicrobial compounds. I'm wondering if anyone has looked into bacterial-communication system (quorum-sensing system) inhibitors which might afford an opportunity to ameliorate bacterial infection by means other than growth inhibition? Actually, to be specific, in addition to VDR transcribed antimicrobial peptides and in conjunction with MP growth inhibition ABXs.
Here's a recent PubMed article on latest compounds capable of overriding bacterial signaling:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687250/pdf/1283-08.pdf
I've setup this thread to discuss the signaling mechanisms {which orchestrate important temporal events during the infection process} and potential antipathogenic drugs or compounds that might specifically target quorum-sensing systems in a manner compatible with the MP and unlikely to pose a selective pressure for the development of resistant strains.
Regards to all,
TikBitten
Last edited on Thu Dec 17th, 2009 21:07 by TikBitten
____________________
Dx:Neurborreliosis 8/05|25D=46 1,25D=62 10/07|Avoid Sun&VitD since 10/07|Started Ph1&NoIRs 3/08|25D=18 3/08|25D=17 6/08|ModPh2 6/08|Ph2 9/08 stopped NoIRs|Ph3 1/09|25D=13 3/09|25D=10 5/09|25D=11 7/09|25D=15 9/09|25D=9 4/11
|
Frans
Member*
|
Posted: Thu Dec 17th, 2009 18:19 |
|
Take a look at Bonnie Bassler's talk for some more background on this. The link is in this thread (search for Bassler):
- http://tinyurl.com/yfk8jg3
She already speculated on a role for quorum sensing with regards to virulence.
Frans
____________________
Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
|
TikBitten
Member
| Joined: | Thu Mar 13th, 2008 |
| Location: | USA |
| Posts: | 81 |
| Status: |
Offline
|
|
Posted: Thu Dec 17th, 2009 19:39 |
|
Read through the material at the link referenced above, made me feel like Johnny come lately. But as you read through the Abstract of the PubMed article I posted atop notice they've since screened hundreds of potential compounds, several with significant "Quorum Sensing Inhibiting" (QSI) in-vivo results. What's interesting is they act synergistically when applied in low dose combination.
"Three compounds, salicylic acid, nifuroxazide, and chlorzoxazone, showed significant inhibition of quorum-sensing-regulated gene expression and related phenotypes in a dose-dependent manner. The results suggest identified compounds have the potential to be used as antipathogenic drugs."
What jumped out at me was "dose dependent manner" and that Salicyclic Acid, or white willow bark, was in the list of studied compounds. While the latter two compounds appear to be prescription pharmaceuticals, Salicyclic Acid is available over the counter. One brand name in the U.S. is "Assalix" and the nice thing it assures a standardized 15% oral dose so you can follow a pre-determined dosing schedule. In that regard two thoughts come to mind:
1) This might be useful in addition to MP ABXs and Benicar therapy.
2) When MP patients need to break from the protocol this might be useful to guard against recurrence and relapse.
Regards,
TB
P.S. Dr. Marshall, notice the use of "Structured Based Virtual Screening" (SB-VS) in lieu of "In-Silico" terminology, interesting...
Last edited on Thu Dec 17th, 2009 22:29 by TikBitten
____________________
Dx:Neurborreliosis 8/05|25D=46 1,25D=62 10/07|Avoid Sun&VitD since 10/07|Started Ph1&NoIRs 3/08|25D=18 3/08|25D=17 6/08|ModPh2 6/08|Ph2 9/08 stopped NoIRs|Ph3 1/09|25D=13 3/09|25D=10 5/09|25D=11 7/09|25D=15 9/09|25D=9 4/11
|
Cynthia Schnitz
Board Staff
| Joined: | Thu Dec 25th, 2008 |
| Location: | N., USA |
| Posts: | 1546 |
| Status: |
Offline
|
|
Posted: Fri Dec 18th, 2009 19:45 |
|
| I guess the only real question that comes to my mind is the question of whether or not quorum sensing in any way affects bacterial survival. I assume that it affects the activity of the bacterial that results in some of the symptoms of disease, but this doesn't sound like a survival thing, tho maybe someone else has some insight into how quorum sensing might help bacterial survival. Seems to me that bacteria have been growing and surviving just fine before they reach the concentration where quorum sensing turns on. Cynthia
____________________
MP start 10/08 (no breaks) | Spondylitis 97, early Diverticulosis 98, early AMD 08, Calcium anomaly 95, TypeII Diabetes(?) 02 | 25D=10.1ng/ml 12/12, (preMP 125D/25D=47/43) | My progress
|
edj2001
Member*
| Joined: | Tue Oct 18th, 2005 |
| Location: | Allen, Texas USA |
| Posts: | 316 |
| Status: |
Offline
|
|
Posted: Mon Dec 21st, 2009 02:38 |
|
These quotes from referenced papers below
“…recent data suggest that some bacterial and eukaryotic signaling mechanisms are closely related…”
“…The bacterium P. stuartii possesses a protein, AarA, that releases it’s quorum-sensing signal… … it is related to the Drosophila melanogaster RHO protein...”
“…Remarkably, AarA and RHO are functionally interchangeable…”
“…introduction of P. stuartii AarA into a D. melanogaster RHO mutant complements the wing development defect, and, introduction of D. melanogaster RHO into a P. stuartii AarA mutant restores quorum sensing…”
“…Interestingly, RHO homologs exist in archaea, bacteria, fungi, plants and humans, suggesting an early and shared evolution of this communication mechanism… “
“…On the basis of the similarity between the mechanism of action of autoinducers in bacterial cells and that of eukaryotic hormones of the nuclear hormone receptor superfamily, we hypothesize that autoinducers function as ligands for as-yet-unknown eukaryotic proteins...”
“…As an initial step in testing this hypothesis, we wished to determine whether autoinducers can indeed efficiently enter mammalian cells. To achieve this goal, we generated a set of chimeric proteins based on LasR and RhlR that could function as sensors of autoinducer action within mammalian cells. Our data demonstrate that both P. aeruginosa autoinducers can efficiently enter and function in mammalian cells…”
“…the mammalian hormone epinephrine can substitute for autoinducer in the QS system of enterohemorrhagic Escherichia coli. Thus, autoinducers and hormones may be interchangeable in a language common to prokaryotes and eukaryotes…”
Urban S, Schlieper D, Freeman M, MRC Laboratory of Molecular Biology, Cambridge, CB2 2QH, United Kingdom. Conservation of intramembrane proteolytic activity and substrate specificity in prokaryotic and eukaryotic rhomboids,
Curr. Biol. 12, 1507–1512 (2002), PMID: 12225666
http://www.ncbi.nlm.nih.gov/pubmed/12225666
Ding X,Baca-DeLancey RR, Siddiqui S, Departments of Medicine and Molecular Biology and Microbiology, Case Western Reserve University School of Medicine,1 and Research Service, Providencia stuartii genes activated by cell-to-cell signaling and identification of a gene required for production oractivity of an extracellular factor,
Journal of Bacteriology, December 1999, p. 7185-7191, Vol. 181, No. 23
0021-9193/99/$04.00+0 (1999)
http://jb.asm.org/cgi/content/abstract/181/23/7185
Gallio M, Sturgill G, Rather P, Kylsten P, Department of Medical Nutrition, Karolinska Institute, and Department of Natural Sciences,
A conserved mechanism for extracellular signaling in eukaryotes and prokaryotes,
Proc. Natl. Acad. Sci. U. S. A. 99, 12208–12213 (2002)
http://www.pnas.org/content/99/19/12208.full.pdf
Williams SC, Patterson EK, Carty NL, Griswold JA, Hamood AN, Rumbaugh KP, Departments of Cell Biology and Biochemistry; Texas Tech University Health Sciences Center; Southwest Cancer Center at UMC, Lubbock, Texas,
Pseudomonas aeruginosa Autoinducer Enters and Functions in Mammalian Cells,
Journal of Bacteriology, April 2004, p. 2281-2287, Vol. 186, No. 8
0021-9193/04/$08.00+0 DOI: 10.1128/JB.186.8.2281-2287.2004
http://jb.asm.org/cgi/content/abstract/186/8/2281
____________________
Sarc98 A.Fib uveitis sk cancer basal/melanoma colon tmr bladder tmr bph| propafenone Armour proscar Guaifensin | 1,25D=50 10/05| 25D=7 4/08| Gene's Story| avd l&D|
|
Joyful
Foundation Staff
| Joined: | Sat Jun 9th, 2007 |
| Location: | North America |
| Posts: | 7001 |
| Status: |
Offline
|
|
Posted: Mon Dec 21st, 2009 18:38 |
|
... the mammalian hormone epinephrine can substitute for autoinducer in the QS system of enterohemorrhagic Escherichia coli ...
So, if I have E. coli where it shouldn't be in my body's tissues and you inject me with an Epi pen, do I get virulence in those tissues? Hmmmm...
____________________
Forums • Be Kind, We Are All Fragile • Conferences
´`•.¸♥¸.•´`•.¸♥¸.•´ `•.¸♥¸.•´`•.¸♥¸.•´`•.¸♥¸.•´`
|
edj2001
Member*
| Joined: | Tue Oct 18th, 2005 |
| Location: | Allen, Texas USA |
| Posts: | 316 |
| Status: |
Offline
|
|
Posted: Mon Dec 21st, 2009 19:19 |
|
The idea that the bacteria produce a chemical (autoinducer) that can interchange with a human hormone as an antagonist or agonist is exactly what Dr Marshall has been saying.
Just think of all the bacteria we have, there are 10X as many bacteria cells as human. These chemicals are finding their way through out our body. Then think about cell wall deficient bacteria inside the cell producing these chemicals with direct access to the nuclear receptors and you can see what a potentinal problem this can be.
When we are born, we should be relatively free of these bacteria (provided we were incubated in a sterile environment). Slowly over time the bacteria collect and multiply and start to influence the function of the nuclear receptors.
Speculating, this maybe the cause of aging and other diseases. For example, maybe these chemicals act as antagonists to the insulin receptors and cause the insulin resistance of diabetes?
The possibilities boggle the mind!!!
Gene
____________________
Sarc98 A.Fib uveitis sk cancer basal/melanoma colon tmr bladder tmr bph| propafenone Armour proscar Guaifensin | 1,25D=50 10/05| 25D=7 4/08| Gene's Story| avd l&D|
|
Dr Trevor Marshall
Foundation Staff
|
Posted: Mon Dec 21st, 2009 19:59 |
|
But we are not incubated in a sterile environment. That is just an old wive's tale...
When you look carefully at this paper:
http://www.pnas.org/content/100/15/8951.long
the exact equivalence between human and pathogenic metabolites becomes crystal clear.
Based on my previous intolerance to epinephrine, and my current tolerance of it (and stress), I find no difficulty accepting the hypothesis that epi stimulates (or signals) the pathogens in some way.
That is more plausible than the hypothesis of specific genetic-predisposition for biochemical dysfunction that everybody else is trying to push...
..Trevor..
|
inuk2600
Member
| Joined: | Mon Oct 12th, 2009 |
| Location: | Manitoba Canada |
| Posts: | 17 |
| Status: |
Offline
|
|
Posted: Tue Dec 22nd, 2009 00:51 |
|
That's inspiring.
I'm so looking forward to my transition back to normal adrenaline tolerance. I can only imagine what a difference that would make.
____________________
CFS symptoms | 25D9(Mar09) | 25D14(Jun09) | 25D6 (Sept11) Ph1Apr09 | Ph2Aug09 | Ph3Jun10 | drop back to Ph1Nov10 | Olmesartan only q6h since early 2011
|
pgeek
Board Staff
| Joined: | Fri Dec 18th, 2009 |
| Location: | Israel |
| Posts: | 2017 |
| Status: |
Offline
|
|
Posted: Thu Dec 24th, 2009 22:24 |
|
Re Cynthia's qn "whether or not quorum sensing in any way affects bacterial survival":
as you say, the bacteria have to be doing quite well before quorum sensing kicks in. But if they do too well they kill their host. So perhaps this mechanism has evolved as way to avoid killing your host - or more generally for shifting into a mode more suitable to continued survival when continued replication would be inefficient (too much competition for food, production of poisonous waste products etc).
So for long term survival it does sound significant.
Perhaps stating the obvious, this quorum-sensing role for epinephrine could also be one of the reasons people on the MP need to be careful with exercise - which amongst other things releases epinephrine. It could also be one of the reasons relapsing illnesses relapse when people get stressed - though I guess plenty of other stress responses could be factors.
____________________
Chronic Prostatitis, IBD(?)|Covered (+ ZnO in sun) |Sunglasses |25D: <4Jan12 (4Mar11/10Dec10/14Jan10| !!!COUCH MUSHROOM DESPERADO!!!
|
Joyful
Foundation Staff
| Joined: | Sat Jun 9th, 2007 |
| Location: | North America |
| Posts: | 7001 |
| Status: |
Offline
|
|
Posted: Fri Dec 25th, 2009 01:22 |
|
_pgeek wrote_
Perhaps stating the obvious, this quorum-sensing role for epinephrine could also be one of the reasons people on the MP need to be careful with exercise - which amongst other things releases epinephrine. It could also be one of the reasons relapsing illnesses relapse when people get stressed - though I guess plenty of other stress responses could be factors.
I've been thinking about that too.
I stumbled on a forum for discussing sleep problems and one person wrote about their problems with tricyclic antidepressents and anything else that increases epinephrine. Their symptoms sounded quite "Th1."
____________________
Forums • Be Kind, We Are All Fragile • Conferences
´`•.¸♥¸.•´`•.¸♥¸.•´ `•.¸♥¸.•´`•.¸♥¸.•´`•.¸♥¸.•´`
|
pgeek
Board Staff
| Joined: | Fri Dec 18th, 2009 |
| Location: | Israel |
| Posts: | 2017 |
| Status: |
Offline
|
|
Posted: Fri Dec 25th, 2009 03:34 |
|
Joyful wrote: I've been thinking about that too.
I stumbled on a forum for discussing sleep problems and one person wrote about their problems with tricyclic antidepressents and anything else that increases epinephrine. Their symptoms sounded quite "Th1."
I think it's been noted here that some antidepressants are antimicrobials. Apparently they're also immunostimulant:
As early as the mid 1980s sufficient evidence had accumulated to be able to state with conviction that lithium and antidepressants have these [immunostimulant] properties. Excessive production of prostaglandin E2 activates microorganisms and suppresses immune function, and lithium and antidepressants oppose prostaglandin E2. From Lithium and antidepressants: stimulating immune function and preventing and reversing infection. http://www.ncbi.nlm.nih.gov/pubmed/17287092
So some of the problems you mention could be IP caused by other mechanisms. Dr Lieb goes on to say:
Immunostimulation is non-specific, possibly relevant to all infections, pertinent to one, two, or more concurrent infections, and highly cost/effective. In controlled studies an antidepressant would be relevant to that agent and only that agent, rendering such studies worthless. Over the past twenty years 22 drug companies have declined interest in developing antidepressants as antiinfectives.
His viewpoint seems rather consistent with the views prevailing here. I couldn't find any references to his name on the site. Perhaps someone should get in touch with him? (His email is in the link above.)
____________________
Chronic Prostatitis, IBD(?)|Covered (+ ZnO in sun) |Sunglasses |25D: <4Jan12 (4Mar11/10Dec10/14Jan10| !!!COUCH MUSHROOM DESPERADO!!!
|
pgeek
Board Staff
| Joined: | Fri Dec 18th, 2009 |
| Location: | Israel |
| Posts: | 2017 |
| Status: |
Offline
|
|
Posted: Fri Dec 25th, 2009 23:43 |
|
Dr Trevor Marshall wrote: When you look carefully at this paper:
http://www.pnas.org/content/100/15/8951.long
the exact equivalence between human and pathogenic metabolites becomes crystal clear. Perhaps this isn't terribly surprising? Single-celled organisms developed quorum sensing as a survival strategy - allowing them to change their behaviour &/ phenotypes depending on group assessments of the environment. With biomolecular mechanisms in place for groups of bacteria to communicate & cooperate, the groundwork for multicellular organisms - and us - was in place.
And any cell-signalling mechanisms bacteria and host animals still have in common will be the easiest for bacteria to exploit. A few mutations and they're in, with significant survival advantages. Some bacterial exploits of host signalling may have come later, from distinct biomolecular origins - but you'd expect the 'easy' exploits to be most common.
I guess another way to look at it is that we're a kind of biofilm. Our hormones, neurotransmitters, cytokines or whatever (& their receptors) are just our quorum-sensing mechanisms... We're just a bit more complicated & forget our humble origins.
____________________
Chronic Prostatitis, IBD(?)|Covered (+ ZnO in sun) |Sunglasses |25D: <4Jan12 (4Mar11/10Dec10/14Jan10| !!!COUCH MUSHROOM DESPERADO!!!
|
TikBitten
Member
| Joined: | Thu Mar 13th, 2008 |
| Location: | USA |
| Posts: | 81 |
| Status: |
Offline
|
|
Posted: Sun Dec 27th, 2009 18:59 |
|
Pgeek-
The conclusion humans are “a kind of biofilm” is a riot! But given a set of opposing thumbs, vertical posture, biped mobility and the ability to recognize myself in the mirror, I’m sticking with the prevailing theory – I'm basically Primate. There’s little doubt, however, that earthly fauna evolved in the presence of microbacterial biofilms as, how, over the past 4 billion years, could they have avoided them? Don’t take my word for it though, feel free to browse around this website http://www.pbs.org/kcet/shapeoflife/episodes/origins_explo2.html and look over the following sentence segment:
…the discovery was made by extracting DNA from a sea sponge and investigating one gene common to all animals. After painstakingly sequencing this gene, Sogin compared its nucleotide sequence (represented by letters i.e. GCAT) to that of the same gene in other animals like worms, mammals, insects and more. Little variation of this gene in different animal groups would signify the groups were closely related while large variations would represent a more distant relationship. After comparing all the groups, he traced out an evolutionary family tree, knowing that the animal at the base of the tree would be our oldest ancestor. He discovered that sponges indeed, were the most basal group that must have laid the foundation for all animal life to follow. "The sponge was the first animal with the genetic blueprint for living large," Sogin says. "All animals are based upon that same blueprint."
So now that we've established some evolutionary distinction between humans and biofilms let’s get back to addressing the context of the discussion thread. Identifying and cataloging quorum sensing inhibitors capable of disrupting biofilm persistence in humans so we get better...
TB
BTW - Speaking of biofilm quorum sensing and evolution here's a link to 2008 Harvard University research on just that topic -> http://sysbio.harvard.edu/csb/foster/joao/pdf/Nadell_QSEvolution.pdf.
I had to read through it a few times before understanding its signficance but, using computer simulations, researches modeled quorum sensing vs. biofilm traits in acute and chronic bacterial infection. Hard to imagine this is what the MP is up against!!!
Last edited on Sun Dec 27th, 2009 23:33 by TikBitten
____________________
Dx:Neurborreliosis 8/05|25D=46 1,25D=62 10/07|Avoid Sun&VitD since 10/07|Started Ph1&NoIRs 3/08|25D=18 3/08|25D=17 6/08|ModPh2 6/08|Ph2 9/08 stopped NoIRs|Ph3 1/09|25D=13 3/09|25D=10 5/09|25D=11 7/09|25D=15 9/09|25D=9 4/11
|
TikBitten
Member
| Joined: | Thu Mar 13th, 2008 |
| Location: | USA |
| Posts: | 81 |
| Status: |
Offline
|
|
Posted: Sun Dec 27th, 2009 19:26 |
|
Cynthia Schnitz wrote: I guess the only real question that comes to my mind is the question of whether or not quorum sensing in any way affects bacterial survival. I assume that it affects the activity of the bacterial that results in some of the symptoms of disease, but this doesn't sound like a survival thing, tho maybe someone else has some insight into how quorum sensing might help bacterial survival. Seems to me that bacteria have been growing and surviving just fine before they reach the concentration where quorum sensing turns on. Cynthia
Cynthia-
Here's an excerpt from a physician website which does a nice job of summing up biofilm pesistence in humans and seems to address your questions...
************
The National Institutes of Health estimates that 60% of all human infections and 80% of refractory infections (unresponsive to medical treatment) are attributable to biofilm colonies. This is common in cases involving pathogen such as Chlamydia pneumoniae, Pseudomonas aeruginosa, Helicobacter pylori, Borrelia burgdorferi (Lyme disease) and Candida albicans.
http://www.advancedhealing.com/blog/wp-content/uploads/2009/09/biofilm.png Fig. 1: The biofilm life cycle. 1: individual cells populate the surface. 2: extracellular polymeric substance (EPS) is produced and attachment becomes irreversible. 3 & 4: biofilm architecture develops and matures. 5: single cells are released from the biofilm.
The protection conferred upon microorganisms by biofilms allows them to achieve a high level of antibiotic resistance, stealth and invisibility. Biofilms not only provide a physical barrier to antimicrobial agents (pharmaceutical antibiotics) and host antibodies, but facilitate the exchange of antibiotic-resistant genetic material between organisms and may contain antibiotic-degrading enzymes such as b-lactamase, effectively neutralizing incoming antibiotic molecules. The decreased growth rate of sessile microorganisms (permanently attached to a substrate and not free to move about) reduces their antibiotic susceptibility as most antimicrobial agents require rapid cell growth in order to effectively kill or inhibit the microbes.
Biofilms thus act much like an “an attached oyster” and render pathogenic microorganisms enormously difficult to eradicate, and can almost single-handedly contribute to localized or systemic inflammatory reactions and delayed wound healing. Depending on the type of biofilm, one or more species of pathogens may be found embedded in the extracellular polymeric substance (EPS). The EPS is composed primarily of polysaccharides and can either stay attached to the cell’s outer surface, or be secreted into its growth medium. Bacterial EPS maybe a carrier of, or may have heavy metals embedded in them, thus, a consideration for chelation w/EDTA.
Pathogenic bacterial known to reside in biofilms include: Borrelia burgdorferi, Escherichia coli, Candida albicans, Clostridium difficile, Clostridium perfringens, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Listeria monocytogenes, Pseudomonas aeruginosa, Salmonella typhimurium, Staphylococcus aureus, Staphylococcus epidermidis, and Vibrio cholerae.
The number of human diseases shown to be associated with biofilms is expanding and includes chronic bacterial prostatitis, chronic rhinosinusitis, cystic fibrosis pneumonia, infective endocarditis, periodontitis, recurrent otitis media, and virtually all device and implant related infections. Strong evidence is also beginning to emerge for an etiologic role of pathogenic mucosal biofilms in gastrointestinal diseases, such as Irritable Bowel Disorders: Crohn’s disease and ulcerative colitis.
And here's the link to his website -> http://www.advancedhealing.com/blog/2009/09/25/dr-ettingers-biofilm-protocol-for-lyme-and-gut-pathogens/
****************
I thought the material might be of interest to you given your earlier post.
Regards,
TBLast edited on Sun Dec 27th, 2009 20:52 by TikBitten
____________________
Dx:Neurborreliosis 8/05|25D=46 1,25D=62 10/07|Avoid Sun&VitD since 10/07|Started Ph1&NoIRs 3/08|25D=18 3/08|25D=17 6/08|ModPh2 6/08|Ph2 9/08 stopped NoIRs|Ph3 1/09|25D=13 3/09|25D=10 5/09|25D=11 7/09|25D=15 9/09|25D=9 4/11
|
Russ
Member*
|
Posted: Sun Oct 17th, 2010 19:55 |
|
edj2001 wrote:
“…the mammalian hormone epinephrine can substitute for autoinducer in the QS system of enterohemorrhagic Escherichia coli. Thus, autoinducers and hormones may be interchangeable in a language common to prokaryotes and eukaryotes…”
Dr Trevor Marshall wrote:
Based on my previous intolerance to epinephrine, and my current tolerance of it (and stress), I find no difficulty accepting the hypothesis that epi stimulates (or signals) the pathogens in some way.
Here is another example of how epinephrine might stimulate the pathogens involved in TH1 disease. This paper shows that the stress hormones epinephrine and norepinephrine are specifically bound by B. burgdorferi, resulting in increased expression of a specific surface protein.
http://www.pnas.org/content/104/17/7247.full.pdf
While the paper is dealing with B. burgdorferi in the spirochetal form and in non-human mammals, I wouldn't be surprised if epinephrine and norepinephrine are also bound by the form that the bacteria takes in chronic human infections, especially given the sensitivity to stress that most people with "Chronic Lyme" experience.
Russ
____________________
*** I recently moved to Connecticut so if anyone knows of MP docs in this state or nearby, please send me a PM. ***
|
Current time is 13:41 | |
|
|
|
|
