Th1-SAIRAUS + KORTISONIN/ARB:N EDUT

[Bb]

Lähettäjä: Soijuv Lähetetty: 25.6.2004 10:50

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Putative Antibacterial Mechanisms for Angiotensin II Receptor Blockers

Authors: Trevor G Marshall, PhD1, Belinda Fenter, BS2, and Frances E Marshall, GradDipPharm, RPh3

Authors Affiliation:
1Autoimmunity Research Foundation, Thousand Oaks, California
2AutoimmunityResearch.org, Fort Worth, Texas
3Los Robles Regional Medical Center, Thousand Oaks, California 91360

email corresponding author: Trevor. m@yarcrip.com
telephone contact: +1-805-492-3693

Date Received: 8 May 2004
Date Published: 9 May 2004
Article Type: Review
Cite this paper as:
Marshall TG, Fenter B, Marshall FE: Putative Antibacterial Mechanisms for Angiotensin II Receptor Blockers. JOIMR 2004;2(2):1

ABSTRACT

Angiotensin II has profound actions in Th1 immune disease. It directly modulates Nuclear Factor-kappaB (NF-kappaB), an essential precursor to the generation of inflammatory cytokines and chemokines, including TNF-alpha.

Corticosteroids exert their anti-inflammatory action by totally shutting down activation of NF-kappaB, while Angiotensin Receptor Blockers (ARBs) inhibit excessive NF-kappaB activation, allowing the phagocytes to respond to immune challenge in a less aggressive manner. The two anti-inflammatory mechanisms are fundamentally different. The new ARB, Olmesartan Medoxomil, has been identified as useful in treating Th1 inflammatory disease sarcoidosis, and the suggestion has been made that ARBs might also directly affect bacterial pathogens. Receptor proteins actively binding angiotensin II have been found on several species of bacteria. We found no match between the human angiotensin receptor and any similar protein in the 294 bacterial genomes currently sequenced, lending credence to the suggestion that bacteria may be using this host hormone in such a manner as to evade the host's immune system. Clearly, if an ARB was capable of actually inhibiting the supply of A-II, thus denying a microbe the ability to protect itself from destruction by phagocytosis, then that ARB could most definitely be classed as an 'antimicrobial'. The dosing of Olmesartan reported as most useful in immunomodulation, 40mg q8h, is well above the level needed to produce maximal hypotensive activity. It would thus seem likely that Olmesartan is acting on atypical receptors, perhaps directly upon pathogens, or upon some yet-to-be-defined human angiotensin-binding-protein(s).
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