Quote from rockarolla on June 18, 2021, 11:49 am

SCFA drops ton of inflammation. The drawback is decreased resistance to infections:

 

Butyrate and other short-chain fatty acids(SCFA) as modulators of immunity: what relevance for health?
https://www.rug.nl/research/pathology/medbiol/pdf/currentopinion_meijer2010.pdf

High-fiber diets have been shown to reduce plasma concentrations of inflammation markers. Increased production of fermentation-derived short-chain fatty acids (SCFAs)is one of the factors that could exert these positive effects. This review examines the effects of SCFAs on immune cells and discusses the relevance of their effects on systemic inflammation, as frequently seen in obesity

SCFAs show anti-inflammatory effects and seem to have the potency to prevent infiltration of immune cells from the bloodstream in, for example, the adipose tissue. In addition, their ability to inhibit the proliferation and activation of T cells and to prevent adhesion of antigen-presenting cells could be important as it recently has been shown that obesity-associated inflammation might be antigen-dependent. More studies with concentrations in micromolar range are needed to approach more physiological concentrations.

High-fiber diet may play a role in controlling the inflammation associated with COVID-19
https://medicalxpress.com/news/2021-03-high-fiber-diet-role-inflammation-covid-.html

In the latest study, healthy colon tissue and epithelial cells were infected with SARS-CoV-2 in the laboratory and subjected to a battery of tests.

"Viral load wasn't reduced and was the same in cells and tissue treated with SCFAs and in untreated samples. However, treated intestinal biopsy samples displayed a significant decrease in expression of the gene DDX58 [an innate immune system receptor that detects viral nucleic acids and activates a signaling cascade that results in production of pro-inflammatory cytokines] and the interferon-lambda receptor, which mediates anti-viral activity. There was also a decrease in expression of the protein TMPRSS2, which is important to viral cell entry," said Raquel Franco Leal, a professor at UNICAMP's School of Medical Sciences (FCM) and co-principal investigator for the study with Marco Aurélio Ramirez Vinolo, a professor at IB-UNICAMP.

https://www.phosphosite.org/proteinAction?id=23939&showAllSites=true
DDX58 Innate immune receptor which acts as a cytoplasmic sensor of viral nucleic acids and plays a major role in sensing viral infection and in the activation of a cascade of antiviral responses including the induction of type I interferons and proinflammatory cytokines. Its ligands include: 5'-triphosphorylated ssRNA and dsRNA and short dsRNA (<1 kb in length).

In addition to the 5'-triphosphate moiety, blunt-end base pairing at the 5'-end of the RNA is very essential. Overhangs at the non-triphosphorylated end of the dsRNA RNA have no major impact on its activity. A 3'overhang at the 5'triphosphate end decreases and any 5'overhang at the 5' triphosphate end abolishes its activity.

Upon ligand binding it associates with mitochondria antiviral signaling protein (MAVS/IPS1) which activates the IKK-related kinases: TBK1 and IKBKE which phosphorylate interferon regulatory factors: IRF3 and IRF7 which in turn activate transcription of antiviral immunological genes, including interferons (IFNs); IFN-alpha and IFN-beta.

[DDX58] Detects both positive and negative strand RNA viruses including members of the families Paramyxoviridae: Human respiratory syncytial virus and measles virus (MeV), Rhabdoviridae: vesicular stomatitis virus (VSV), Orthomyxoviridae: influenza A and B virus, Flaviviridae: Japanese encephalitis virus (JEV), hepatitis C virus (HCV), dengue virus (DENV) and west Nile virus (WNV).

It also detects rotavirus and reovirus.

Also involved in antiviral signaling in response to viruses containing a dsDNA genome such as Epstein-Barr virus (EBV).

Short chain fatty acid butyrate promotes virus infection by repressing interferon stimulated genes
https://www.biorxiv.org/content/10.1101/2020.02.04.934919v1.full

[2004] Sodium butyrate suppresses interferon-gamma-, but not lipopolysaccharide-mediated induction of nitric oxide and tumor necrosis factor-alpha in microglia
https://www.jni-journal.com/article/S0165-5728(04)00074-8/fulltext
In the present study, we demonstrate that sodium butyrate repressed IFN-γ-induced expression of iNOS and TNF-α, but had little effect on LPS-induced expression in BV2 murine microglial cells. Sodium butyrate significantly inhibited NF-κB binding and NF-κB-mediated transcription induced by IFN-γ, suggesting that the anti-inflammatory effect of sodium butyrate is mediated via specific inhibition of the NF-κB pathway. IFN-γ is a major stimulator of innate and adaptive immune response. Thus, the specific down-regulation of IFN-γ-induced microglial activation by sodium butyrate may provide potential therapeutic strategies for a variety of inflammatory diseases in the central nervous system.
...
Butyrate is a four-carbon fatty acid normally produced as a result of bacterial fermentation of fiber in mammalian intestines.
...
In order to further investigate an anti-inflammatory role of sodium butyrate in the brain, this study examined the effect of sodium butyrate on microglial activation. Here, we report for the first time that sodium butyrate attenuates IFN gamma-mediated induction of NO and TNF via inhibition of NFnB activation. Thus, the selective modulation of IFN-gamma specific pathway by sodium butyrate may provide a novel framework for defining the differential activation mechanisms of microglia and development of a disease-specific therapeutic target for various neuronal diseases associated with microglial activation.

Sodium butyrate suppresses the expression of TNF-a induced by IFN-gamma

TNF-a is another major molecule induced by various inflammatory stimuli, and it plays a central role in various inflammatory diseases (Meda et al., 1995). BV2 cells were stimulated with LPS (100 ng/ml) or IFN-g (20 U/ml) in the presence or absence of sodium butyrate.

https://en.wikipedia.org/wiki/Interferon_gamma
IFNγ, or type II interferon, is a cytokine that is critical for innate and adaptive immunity against viral, some bacterial and protozoal infections. IFNγ is an important activator of macrophages and inducer of Class II major histocompatibility complex (MHC) molecule expression. Aberrant IFNγ expression is associated with a number of autoinflammatory and autoimmune diseases. The importance of IFNγ in the immune system stems in part from its ability to inhibit viral replication directly, and most importantly from its immunostimulatory and immunomodulatory effects. IFNγ is produced predominantly by natural killer (NK) and natural killer T (NKT) cells as part of the innate immune response, and by CD4 Th1 and CD8 cytotoxic T lymphocyte (CTL) effector T cells once antigen-specific immunity develops[11][12] as part of the adaptive immune response. IFNγ is also produced by non-cytotoxic innate lymphoid cells (ILC), a family of immune cells first discovered in the early 2010s.

Quote from lil chick on June 29, 2021, 6:56 am

I was thinking about gum disease in VA toxicity, and I think it might actually be more about *wrong bone formation* than about germs.  In VA toxicity, bone is taken away from where it is supposed to be and ends up where it isn't supposed to be.

I was talking once to the holistic dentist in my town about gum disease and what they said is that the *roughness* has to go for the gum to re-attach.  The teeth are coated with rough stuff (which is I guess is what they call plaque) and which is removed by the hygienist with her little scraper thing.  If you saw the tooth under a microscope it would be crazy rough-- like little crystals.

This roughness even extends a bit below the gum line causing the soreness and the recession.

I think I can feel (with my tongue) that some of my teeth *are* now smoother (at 2 years in), while problematic areas still have some roughness.   I also feel the roughness (in the problematic areas) with the dental floss--it doesn't slide as easily.

Personally, I think even if you don't go to the hygienist for cleanings,  that the body will figure out the roughness by itself as you detox and your bone formation returns to normal.  ?  But I could be wrong.

I think that daily cleanliness helps because it physically removes a small amount of the VA from the mouth with the detergents in toothpaste, the bubbling action of peroxide, the friction of brushing and flossing and so on.   Think of it:  this is where most of the VA's enter the body!  Of course some would have absorbed in the mouth.   I think it is probably a good idea to let the toothpaste be in the mouth a minute or two so that the soaps or detergents can do their work.  Don't be in a hurry and don't be shy with the product.  Frictiony additives in toothpaste might be a nice idea,, like baking soda.

I once saw a video about *tapping* the teeth with the brush at the gum line, and I can see how that might help reduce roughness over time.  I haven't instituted this habit yet. 

When @ourania talks about detoxed lymph from the brain coming out between the teeth I kind of freak out!   But hey, I'm not adverse to thinking that could be happening.  But what's the damn body thinking?     Wouldn't the lymph then have to go through the whole digestive system and possibly retox on the way?    But I do have weird gunk form up between my teeth and it isn't always apparent that it's from food.  So I have instituted a "no-excuses" flossing routine.  I sort of hate flossing but I want that stuff OUT.