Wonder who's brain they used? Their own?

Infect Immun. 2005 Feb;73(2):1014-22.

Borrelia burgdorferi, host-derived proteases, and the blood-brain barrier.

Grab DJ, Perides G, Dumler JS, Kim KJ, Park J, Kim YV, Nikolskaia O, Choi KS, Stins MF, Kim KS.

Department of Pediatrics, The Johns Hopkins University School of Medicine, Park Building, Room 256, 600 North Wolfe Street, Baltimore, MD 21287, USA. [email protected]

Neurological manifestations of Lyme disease in humans are attributed in part to penetration of the blood-brain barrier (BBB) and invasion of the central nervous system (CNS) by Borrelia burgdorferi.

However, how the spirochetes cross the BBB remains an unresolved issue. We examined the traversal of B. burgdorferi across the human BBB and systemic endothelial cell barriers using in vitro model systems constructed of human brain microvascular endothelial cells (BMEC) and EA.hy 926, a human umbilical vein endothelial cell (HUVEC) line grown on Costar Transwell inserts.

These studies showed that B. burgdorferi differentially crosses human BMEC and HUVEC and that the human BMEC form a barrier to traversal. During the transmigration by the spirochetes, it was found that the integrity of the endothelial cell monolayers was maintained, as assessed by transendothelial electrical resistance measurements at the end of the experimental period, and that B. burgdorferi appeared to bind human BMEC by their tips near or at cell borders, suggesting a paracellular route of transmigration.

Importantly, traversal of B. burgdorferi across human BMEC induces the expression of plasminogen activators, plasminogen activator receptors, and matrix metalloproteinases.

Thus, the fibrinolytic system linked by an activation cascade may lead to focal and transient degradation of tight junction proteins that allows B. burgdorferi to invade the CNS.

At least it is certainly a lot easier to understand!

It is my understanding that TNF alpha plays a part in lowering the BBB...maybe done for some protective reasons:

Even dysregulation of the blood brain barrier (BBB) is seen early in neuroinflammation, and parallels the release of proinflammatory cytokines [26-28]. Mechanisms for disruption of the BBB in neuroinflammation are incompletely understood, but appear to involve direct effects of cytokines on endothelial regulation of BBB components.

Exposure of endothelium to TNF-� interrupts the BBB by disorganizing cell-cell junctions. Furthermore, TNF-� has been shown to depress calcium (Ca2+) signaling between BBB endothelial cells by reducing gap junction coupling and inhibiting triggered ATP release [29].
http://www.jneuroinflammation.com/content/1/1/22

Re: TNF alpha:

4. ``is actually a potent modulator of neurotransmitter interaction.''

hdlighthouse.org/see/immune/tnf.htm

5. ``the body does use tumor necrosis factor-alpha (TNF-alpha) to acutely fight infections. If patients
are showing any sign of infectious disease, drugs such as Enbrel (that inhibit the effects of TNF-alpha) are temporarily discontinued.''
www.lef.org/protocols/prtcl-128a.shtml

11. ``the level of TNF-alpha directly or indirectly regulates the production of borreliacidal antibody''

PMID: 12522038

***13. ``no detrimental effects on normal neurons and can protect neurons when present in neuronal cultures during in vitro ischaemia...Once TNF's removed, neuroprotection is lost.''
www.anri.uwa.edu.au/teams/teamcvdl/cvdl.htm
---------------

3. ``Severe Mg deficiency *changed mineral homeostasis, *induced membrane damage, increased lipid peroxidation and cytokine concentrations and reduced immunocompetence.''
PMID: 9558736

a left at the TMJ junction

and a hard U turn at the frontal lobe.

Yup.

I vote for that last explanation.

Doesn't it make you feel good to know that not only did your immune system not kill the darn bug...but it actually gave it a ride across the most defended barriers in your body?

no matter which they use,i know they like this hotel/motel.i must be a 5***** rating....gary

Thanks for posting this, Tincup.