There are many immunological differences in humans and mice (follow my link) that are never discussed — not even in Science 2015;349/6252:1106.
Ignoring the long-standing paradox that endotoxin is also acting as a natural adjuvant to atopic inflammation, the credibility of the Science paper is further reduced.
IMHO it is also a strange experimental condition to have all animals on a standard vitamin D diet – a known co-sensitizers – and looking then for A20 which is co-regulated by vitamin D ??
And here is the last argument – more than 90% of studies in mice fail to translate into humans.
I have probably two candidates here. The first one is by the Cantorna group in October 2013 and provides for the first time a link between between the gut microbiome and oral vitamin D exposure. We all thought that vitamin D has no influence on bacteria as they cannot utilize it. But that doesn’t seem to be true as the composition of the microbiome may change.
Mice that cannot produce 1,25(OH)2D3 [Cyp27b1 (Cyp) knockout (KO)], VDR KO as well as their wild-type littermates were used. Cyp KO and VDR KO mice had more bacteria from the Bacteroidetes and Proteobacteria phyla and fewer bacteria from the Firmicutes and Deferribacteres phyla in the feces compared with wild-type. In particular, there were more beneficial bacteria, including the Lactobacillaceae and Lachnospiraceae families, in feces from Cyp KO and VDR KO mice than in feces from wild-type … Our data demonstrate that vitamin D regulates the gut microbiome and that 1,25(OH)2D3 or VDR deficiency results in dysbiosis, leading to greater susceptibility to injury in the gut.
So while I always thought, oral vitamin D supplementation may have a direct effect on the gut mucosal system, this paper opens a completely new avenue. The best vitamin D paper in 2013 weiterlesen