That's interesting. The vaccine isn't what they are crediting with reversal of diabetes or multiple sclerosis. It's the TNF. Which...drum roll please...inhibits aldosterone production!
http://endo.endojournals.org/content/125/6/3084.shortQuote:
Tumor Necrosis Factor and Interleukin-1 Are Potent Inhibitors of Angiotensin-II-Induced Aldosterone Synthesis*
R. NATARAJAN,
S. PLOSZAJ†,
R. HORTON and
J. NADLER‡
- Author Affiliations
Section of Endocrinology, University of Southern California-Los Angeles County Medical Center Los Angeles, California 90033
Address requests for reprints to: Rama Natarajan, Ph.D., Section of Endocrinology, University of Southern California Medical Center, Room 18632, 2025 Zonal Avenue, Los Angeles, California 90033.
Abstract
Cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1), mediate many inflammatory and cellular responses. However, the effects of TNF and IL-1 on basal and angiotensin-II (All)-stimulated aldosterone synthesis are not known. We studied the effect of recombinant and purified TNF and IL-1 on basal as well as All-, ACTH-, and K+-induced aldosterone synthesis in isolated rat adrenal glomerulosa cells. Since we have previously shown that All action is mediated by activation of the 12-lipoxygenase (12LO) pathway of arachidonic acid, we also evaluated the effects of these cytokines on the 12LO product 12-hydroxyeicosatetraenoic acid (12HETE) using a validated RIA technique. TNF at 2.5 and 5.0 ng/ml produced a dose-dependent inhibition of All-induced aldosterone synthesis [All, 39.0 ± 3.3 ng/106 cells-h; All plus TNF (5.0 ng/ml), 14.3 ± 1.6; P < 0.001 vs. All; All plus TNF (2.5 ng/ml), 24.7 ± 3.2; P < 0.01 vs. All]. Similarly, TNF at 5.0 ng/ml also attenuated the stimulatory effect of ACTH (10−9 M). However, K+- induced aldosterone synthesis was not altered. TNF also did not alter basal aldosterone levels. All, as previously shown, stimulates 12HETE synthesis (basal, 608 ± 114 pg/105 cells-h; versus All, 1268 ± 197; P < 0.02). TNF at concentrations of 1.0–5.0 ng/ml produced a dose-dependent inhibition of All stimulatory action on 12HETE synthesis [All plus TNF (1.0 ng/ml), 650 ± 26 pg, P < 0.03 vs. All; All plus TNF (5.0 ng/ml), 390 ± 46; P < 0.01 vs. All plus TNF (1.0 ng/ml)]. In addition, 12HETE at 10−8 M completely restored the effects of All during blockage by TNF. Purified human IL-1 (75% β, 25% α) as well as recombinant human IL-1β at concentrations as low as 50 pg/ml inhibited All-induced aldosterone synthesis. IL-1β did not alter ACTHor K+-induced aldosterone synthesis and, in fact, had a tendency to potentiate ACTH effects. These results suggest that the cytokines TNF and IL-1 are potent inhibitors, particularly of All action in the adrenal glomerulosa cell. Therefore, local or systemically produced TNF or IL-1 may be important negative modulators of aldosterone synthesis.
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