Vitamin B5 boosts the immune response

[cs3000]

Vitamin b5 stimulates the immune system through increasing IL-22 T cells

Immunostimulatory effects of vitamin B5 improve anticancer immunotherapy

Vitamin B5 (panthotenic acid), the precursor of coenzyme A (CoA), is contained in most food items and is produced by the intestinal microbiota. A recent study published in Cell Metabolism reports that vitamin B5 and CoA favor the differentiation of CD8[+] ...

www.ncbi.nlm.nih.gov

A recent study published in Cell Metabolism reports that vitamin B5 and CoA favor the differentiation of CD8+ cytotoxic T cells into interleukin-22 (IL-22)-producing Tc22 cells, likely through fueling mitochondrial metabolis

Patients in the highest tertile of plasma B5 levels exhibited the highest survival with respect to time to next treatment as compared to patients with intermediate and low B5 levels

Interleukin-22 Inhibits Respiratory Syncytial Virus Production by Blocking Virus-Mediated Subversion of Cellular Autophagy

Respiratory syncytial virus (RSV) infection can cause severe bronchiolitis in infants requiring hospitalization, whereas the elderly and immunocompromised are prone to RSV-induced pneumonia. RSV primarily infects lung epithelial cells. Given that no vaccine against RSV is currently available, we tested the ability of the epithelial-barrier protective cytokine interleukin-22 (IL-22) to control RSV production. When used in a therapeutic modality, IL-22 efficiently blunted RSV production from infected human airway and alveolar epithelial cells and IL-22 administration drastically reduced virus titer in the lungs of infected newborn mice. RSV infection resulted in increased expression of LC3B, a key component of the cellular autophagic machinery, and knockdown of LC3B ablated virus production.
RSV subverted LC3B with evidence of co-localization and caused a significant reduction in autophagic flux, both reversed by IL-22 treatment. Our findings inform a previously unrecognized anti-viral effect of IL-22 that can be harnessed to prevent RSV-induced severe respiratory disease.

The RDA for b5 intake might be irrelevant. apparently most b5 is produced in the gut. colitis often comes with b5 deficiency.
Vit D deficiency might also cause a b5 deficiency (?) paradoxically upping vit d might also (?)


interestingly theres no transport saturation for high dose b5 unlike many of the b vits. with high dose all gets taken up

pro immunity effect, switches to anti infection at later stages. (maybe best not to take this with inflammatory conditions? personally didnt help my colitis much if at all.) but apparently opposite effect in early stages.

As a paradoxical effect on cytokines, VB5 endorses neutrophils to produce anti‐inflammatory cytokines to slow down the recruitment
or activation of macrophages in early infection but stimulates the secretion of proinflammatory cytokines to enhance
their recruitment or activation in late infection (He et al., 2018). VB5 promoted the maturity of macrophages and phagocytosis and strengthened their potential activation status

Vitamin B5 Reduces Bacterial Growth via Regulating Innate Immunity and Adaptive Immunity in Mice Infected with Mycobacterium tuberculosis in vivo mice study , boosted pro immune cytokine response in response to bacterial infection

(effect size not big in bacteria model but there. wonder what its like against viruses)

human dose 500mcg (vb1 typo, its vb5)
(the dose is a typo too, 10mcg per 100g bodyweight is way too low
im gonna take it as 500mg human for pro immunity response)