The Specific Effect Ketones have on the Immune Response (Good and Bad)

Date: 2020-04-07 14:30:04

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The Specific Effect Ketones have on the Immune Response (Good and Bad) – Thomas DeLauer

Our immune system is dependent on its ability to recognize foreign particles. Besides, it is also able to detect physiological processes induced by infection like dysregulated proton balance inside the cell. Too little stimulation of the IS and there is no response to the pathogen – too much of a stimulation and dysregulated inflammation can cause fibrosis of lungs which consequently lose the ability to transport oxygen into our bodies.

The role of the NLRP3 inflammasome in responses to influenza An infection is a perfect example of the balance concept. NLPR3 inhibition is discussed in the keto community as beta-hydroxy-butyrate, the primary ketone, was reported to be able to inhibit NLRP3. However, to critically evaluate the potential benefits and risks of such NLRP3 inhibition, we need to assess the pathway with all its impacts.

NLRP3 stands for nod-like receptor protein 3 and is activated by double-stranded RNA. It is involved in the maturation of pro-inflammatory cytokines IL-1 and IL-18. These cytokines act as promoters of what is called the acute-phase immune response. IL-1 is responsible for the recruitment of monocytes, macrophages and neutrophils and T-cells. From these 4 kinds of cells, only T-cells are pathogen-specific and provide the most efficient defence. However, T cells must reproduce first which takes time. The other cells are part of the innate immune system and their main advantage is that they act quickly. Imagine T cells as snipers, who are very efficient in who they kill but it takes them time to aim and their training takes time as well. In comparison, monocytes, macrophages and neutrophils are like bombardiers.

The protective effect of the inhibitor is especially important for highly pathogenic and pandemic viral strains which contain special virulent factors which induce “second wave” of inflammation. Stopping this through inhibition of NLRP3 might protect against pathophysiological inflammatory damage of lungs and might explain for the decreased lethality after administering the NLRP3 inhibitor later on.

A study published by Nature Scientific Reports connects NLRP3 with a ketogenic diet. It reported that Beta-hydroxy-butyrate (BHB) is an NLRP3 inhibitor.

Role of BHB in more immunological setting was examined in a study published in Nature Medicine. Mice were genetically engineered to possess the same mutation as patients with Muckle-Wells Syndrome or Familial Cold Autoinflammatory syndrome. This mutation makes the NLRP3 active even in the absence of its ligands (e.g. viral particles), resulting in chronic inflammation. BHB was able to block these diseases, most probably by inhibiting NLPR3. Indeed, decreased levels of IL-1 were observed in BHB treated mice.

As mentioned previously, they need their host’s cells to replicate. They use our ribosome to translate their DNA or RNA into structural proteins like spike proteins which are essential for entry to the host cell by injecting its virion into the cytosol. In addition, the it also needs to create its capsule which is made out of phospholipids. To do this, the “hijacks” the process of de novo fatty acid synthesis. This is such an important step in the replication that inhibitor of fatty acid synthase called C75 showed a potent antiviral effect.

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