high salt intake and TGF-B1

[Guest guest]

" Administration of 8.0% NaCl diet to rats for 7 days did not affect

blood pressure but increased steady-state mRNA and protein levels of

NOS3 in the arterial wall compared with animals on 0.3% NaCl diet.

Northern analysis demonstrated increased steady-state amounts of mRNA

of TGF-beta1 in aortas of rats on 8.0% NaCl diet. "

I have no knowledge on whether it's safe for people to take gobs of

salt (or vitamin C)...

Nor any knowledge on whether the TGF-B1 concentration changes

discussed in this abstract would affect symptoms or control of

bacteria...

I glanced at one paper suggesting that overproduction of TGF was a

factor in the ability of Mtb to walk over the immune system. We've

talked here before about something similar involving Mtb and IL-10.

TGF inhibitors have apparantly been tested in cancer. I took a quick

look and didn't turn up any reports of herxing. You'd think that if

some immunomodulatory drug were to accidentally turn out to be highly

effective for intracellular bacterioses that might cause some chronic

diseases, at least a few people in the trials with a mild CFS/etc

disease (perhaps not even diagnosed) would probably be herxing on it.

Whether that would show up in the lit (not as a herx, of course, but

as some strange adverse reaction) is less clear, because doctors

might just say, oh, this person felt crappy on the drug, that kind of

thing happens. Which it does, alot. Perhaps a herx would be most

likely to be reported (again, not as such) in MS, since herx-like

reactions reported by MS patients using abx sometimes include

specific neurologic symptoms rather than just feeling ill.

========full abstract quoted from above==========

Am J Physiol. 1999 Oct;277(4 Pt 2):H1293-8. Links

Dietary salt increases endothelial nitric oxide synthase and TGF-

beta1 in rat aortic endothelium.Ying WZ, PW.

Nephrology Research and Training Center, Comprehensive Cancer Center,

Division of Nephrology, Department of Medicine, Birmingham, Alabama

35233, USA.

The amount of NaCl in the diet plays an important role in modulating

nitric oxide (NO) synthesis in vivo. In the glomerulus, dietary NaCl

also regulates transforming growth factor-beta1 (TGF-beta1)

production. We hypothesized that dietary NaCl intake regulated

expression of the endothelial isoform of nitric oxide synthase (NOS3)

and TGF-beta1 in the aorta. Administration of 8.0% NaCl diet to rats

for 7 days did not affect blood pressure but increased steady-state

mRNA and protein levels of NOS3 in the arterial wall compared with

animals on 0.3% NaCl diet. Northern analysis demonstrated increased

steady-state amounts of mRNA of TGF-beta1 in aortas of rats on 8.0%

NaCl diet. By ELISA, both total and active TGF-beta1 were increased

in these vessel segments. Endothelial denudation of aortic rings

reduced active TGF-beta1 secretion to undetectable levels. Addition

of a neutralizing antibody to TGF-beta to aortic ring segments

attenuated NO production but not to that observed in animals on the

0.3% NaCl diet. The data showed that dietary NaCl intake modulated

NOS3 and TGF-beta1 expression in the arterial wall; NOS3 expression

was at least partially regulated by endothelial cell production of

TGF-beta1.

PMID: 10516163