Three papers on trained immunity, with the first a 2021 review:
“Trained immunity is realized by epigenetic reprogramming of cells, primarily monocytes/macrophages and natural killer cells, and is less specific than adaptive immunity. It may cross-protect against other infectious agents.
Various actions of trained innate immunity on precursor cells have a strong potential for therapeutic use, particularly in infected and myelosuppressed individuals. Improvements of effects of some vaccines offer other potential use of β-glucan as an inductor of trained immunity, suggesting novel uses of a traditional therapeutic.”
https://www.mdpi.com/1422-0067/22/19/10684/htm “Trained Immunity as an Adaptive Branch of Innate Immunity”
Became tired of this review’s pedantic repetitions, that cells have a finite existence, as do cell attributes such as one-time trained immunity. Readers get it.
While belaboring the obvious, this paper missed two points:
- As An environmental signaling paradigm of aging theorized, then demonstrated in A rejuvenation therapy and sulforaphane, and continues in current studies, cells take on phenotypes the body gives them. Focusing on cell attributes missed many signals elsewhere in cells’ environmental milieu, which make a difference in cell, organ, and body functioning.
- Trained immunity protocol also matters. I’ve trained my immune system with yeast cell wall β-glucan every day for 17 years, recently taking nothing else an hour before or an hour after. That “no effects were found after 20 days” of only one in vitro dose isn’t relevant to my immune responses. I always have cells with one day of training, cells with (pick a number) days / weeks / months / years of training, and millions of primed cells in between.
This first paper cited a 2020 in vitro study:
“(1, 3)/(1, 6)-β-glucan can induce potent trained immunity, however, immunoregulatory activity of oat (1, 3)/(1, 4)-β-glucan has been neglected. Most studies have focused on its metabolic regulatory activity in diseases such as obesity and diabetes.
This study confirmed that β-glucan from oat dietary fiber can modulate responsiveness of innate immune cells through metabolic reprogramming. Proposed mechanism of oat β-glucan for trained immunity induction in monocytes/macrophages:
This study showed that trained immunity induced by oat (1, 3)/(1, 4)-β-glucan was dependent on glycolysis or SDH/IRG axis in TCA cycle. These findings demonstrated that oat dietary fiber could strengthen and maintain long-term responsiveness of the innate immune system.”
https://doi.org/10.1007/s10753-020-01211-2 “Oat-Derived β-Glucans Induced Trained Immunity Through Metabolic Reprogramming” (not freely available)
A 2021 rodent study cited this second paper:
“Oat beta-glucans can stimulate secretion of anti-inflammatory cytokines, and simultaneously inhibit secretion of pro-inflammatory cytokines. The immunostimulatory effect of beta-glucan intake occurs due to its ability to activate intestinal mucosa immune cells, which results from binding of these polysaccharides to specific membrane TLR and/or Dectin-1 receptors.
We analyzed effects of oat beta-glucans at two time points, 3 and 7 days after TNBS administration:
- High molecular mass beta-glucan forms a protective coating on the internal intestinal wall, which improves tissue recovery potential and reduces the risk of secondary microbial infection.
- Low molar mass beta-glucan forms light solutions where short chains are well distributed and dispersed, and due to low viscosity, beta-glucan is accessible for receptors to be reached. Once reaching and complementing the receptor, bonded beta-glucan short polymeric chain induces transmission on metabolic pathways.
Consumption of oat beta-glucans reduced levels of inflammatory markers, and recovered signaling pathways and histological changes, with stronger effects of low molar mass beta-glucan after 7 days of colitis. Dietary oat beta-glucans can reduce colitis at the molecular and organ level, and accelerate Crohn’s disease remission.”
https://www.mdpi.com/1422-0067/22/9/4485/htm “Anti-Inflammatory Activity of Oat Beta-Glucans in a Crohn’s Disease Model: Time- and Molar Mass-Dependent Effects”
I’d seen this second study’s abstract several times, but glossed over it. I curated another 2021 rodent study from the same institution as this third paper in Oat β-glucan effects on colitis.
None of these studies investigated gut microbiota. Pretty sure our hosted microorganisms had roles in their findings.
All papers called for human studies of their findings. But it would be difficult for drug companies to make money from a research area that’s cheap and readily accessible. Take responsibility for your own one precious life.