The Stealth Killer: Is Oral Spirochetosis the Missing Link in the Dental and Heart Disease Labyrinth?

The Stealth Killer: Is Oral Spirochetosis the Missing Link in the Dental and Heart Disease Labyrinth?

http://www.amazon.com/Stealth-Killer-Spirochetosis-Missing-Labyrinth/dp/0976379783/ref=sr_1_1?ie=UTF8&qid=1305525311&sr=8-1

“The authors may have found the missing link between medicine and dentistry in general, and between oral spirochete infection and chronic inflammatory diseases in particular.

The chapter on the use of spirochetes as biological warfare is fascinating, making one wonder about the origin of the current epidemic of Lyme disease.

The chapter on Vitamin D reminds one to be careful about the recommendation of Vitamin D in the current Vitamin D deficiency ‘epidemic’.

The Silent Saboteurs:
Unmasking Our Own Oral Spirochetes As The Key To Saving TRILLIONS in Health Care Costs

http://www.lymebook.com/ss-sample-chapter.pdf

http://www.lymebook.com/silent-saboteurs-nordquist-krutchkoff

http://www.amazon.com/Silent-Saboteurs-Unmasking-Spirochetes-Trillions/dp/0982513852/ref=pd_sim_b_4

"This is a story about a very special group of bacteria; uniquely different and interesting microbes that live within our mouths. These peculiar forms of life, known collectively as oral spirochetes, are unknown to most and misunderstood by nearly all. We have a story to tell concerning a proposed role these microbes play as saboteurs of our body defenses

Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
Cabral ES, Gelderblom H, Hornung RL, Munson PJ, Martin R, Marques AR.
Source

Clinical Studies Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-1888, USA.
Abstract

Toll-like receptors (TLRs) trigger innate immune responses via the recognition of conserved pathogen-associated molecular patterns. Lipoproteins from Borrelia burgdorferi, the agent of Lyme disease, activate inflammatory cells through TLR2 and TLR1. We show that stimulation of human monocytes with B. burgdorferi lysate, lipidated outer surface protein A, and triacylated lipopeptide Pam3CysSerLys4 results in the up-regulation of both TLR2 and TLR1 but the down-regulation of TLR5, the receptor for bacterial flagellin, and that this effect is mediated via TLR2. TLR4 stimulation had no effect on TLR2, TLR1, and TLR5 expression. Human monocytes stimulated with TLR5 ligands (including p37 or flaA, the minor protein from B. burgdorferi flagella) up-regulated TLR5. In addition, TLR2 stimulation rendered cells hyporesponsive to a TLR5 agonist. These results indicate that diverse stimuli can cause differential TLR expression, and we hypothesize that these changes may be useful for either the pathogen and/or the host.

Most strikingly, TLR5 functionality was halted in our EBV-infected cells ...

tooyoung wrote:Whats the best way to stop the oral spirochetes?