Re: antibiotic therapy reducing gut ...Nelly's Abstract

[Guest guest]

Yeah! Nelly, struggling or not you do have a way of coming up with

the goods. I must have been craving a nice, clear, broadly focused

abstract like this. It is hot off the press, and addresses so much

of what we've been discussing!

Makes me very proud of this list, how we seem to be moving on a

parallel track with the research.

I hope will have a gander at this abstract, and edify us all

with some apt comment.

I don't know about cysts, but blebs have been accused even by Steere

of causing protracted inflammation.

I hope you're coming out of the difficulty from Flagyl?

>

> [infections] Re: antibiotic therapy

reducing gut microflora

>

>

>

> PAUL ASKS:

> > I'm not as polite as Donta, so I'll repeat my question: in

your

> > opinion, does medical science " know " what cysts are, how they

> relate

> > to sickness or recovery?

>

> BARB REPLIES:

> From reading the literature, I think:

>

> They know cysts are a variant form, they know that samll

spirochete

> (or multiple chetes) can emerge from within a cyst (which is

very

> interesting), they know the cyst form has additional/different

cell

> wall proteins from the parent form and is many layered, and

they

> know know the cyst form is a sucessfull survival mechanism -

>

> but no, they do not know how cysts relate to sickness or

recovery in

> regards to say... which is worse symptomactically - a colony of

> classical spirochetes - or a gaggle of cysts.. not that I've

read

> anywhere anyway.

>

> PAUL ASKS:

> >

> > I've seen studies discussing in a very matter of fact way that

> > cystic forms of borrelia survive antibiotic treatment. What I

am

> > unsure of is whether in describing these residual organisms

the

> > researchers are employing some clear and agreed upon

understanding

> > of what the " cyst form " represents.

>

>

> BARB REPLIES:

> Sort of the same question.

> In terms of survival of the organism, in protein make up, yes.

> In contribution to disease symptoms, no.

>

> NELLY says:

>

> I think I did read that " Bb cysts " did cause inflammation by

triggering the production of pro-inflammatory cytokines (don't quote

me, I feel too tired to look anything up). In the Polish study below

I am not sure whether they make the distinction btwn sxs caused by

Bb in spiro form and Bb in cystic, bleb-format but I have read some

place that blebs (if not cysts) cause irritation of something or

other

> Nelly (struggling)

>

> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=12194230

>

> Przegl Epidemiol. 2002;56 Suppl 1:57-67. Related

Articles, Links

>

>

> [New aspects of the pathogenesis of lyme disease]

>

> [Article in Polish]

>

> Zajkowska JM, Hermanowska-Szpakowicz T.

>

> Klinika Chorob Zakaznych i Neuroinfekcji AM w Bialymstoku.

>

> Morphological changes of B. burgdorferi as well as changes in

expression of surface proteins caused by environmental determinants

are essential in pathogenesis of Lyme disease. Cysts, spherical form

(spheroplasts, L-form) and " blebs " (gemmae) can be responsible for

long lasting antigenic stimulation, signs of chronic borreliosis,

and even probably connected with MS and Alzheimer disease.

Mechanisms to avoid elimination and persistence in the host include:

expression of low heterogenic Osp A, B replaced by polymorphic in

sequence and antigenic reactivity OspC, the hindrance of access to

some membrane proteins by other proteins on the spirochete's

surface, effects of tick saliva proteins action. Hiding of

spirochetes is possible by invagination into fibrocytes membrane as

well as, coating by antigens derived from lymphocytes B.

Distribution of spirochetes is facilitated by binding to platelets

through integrin aIIb b3, and to the endothelial cells through

integrins av b3 i a5b1, recognition of decorin by lipoproteins DbpA

i DbpB, receptor for NAG (N-acetyl glucosamina). Endothelial cells,

toxic products of granulocytes, monocytes, macrophages as well as

phagocytosis counterpart in pathogenesis. Induced cytokines are

connected with activation subsets of T lymphocytes involved in

inflammatory response. Cytokines produced by Th1 as cytotoxic CD8

accompany the disease. Important are also dendritic cells regarded

as initiators of Th1 response with participation of IL-12. In

pathogenesis of Lyme disease participation of autoimmunity is

notified, especially molecular similarities between OspA and human

lymphocytic antigen (hLFA-1). Neurotoxin, produced by B. burgdorferi

Bbtox1 was identified. Encephalopathy signs in Lyme borreliosis

could be result of releasing toxico-metabolic products, ability of

spirochetes to pass the blood-brain barrier as well as, effect of

lymphocytes migration. Active invasion of brain endothelium as

ability to adherence to endothelial wall could be the source of

focused or disseminated inflammation of brain vessels. Antiaxonal

antibodies could disturb axon conduction without damaging. But

damage of white matter could be connected with damage of mielin

production cells, probably by antibodies, induced in cross reaction.

>

> Publication Types:

> a.. Review

> b.. Review, Tutorial

>

> PMID: 12194230 [PubMed - indexed for MEDLINE]