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.
A report in Biospektrum 07.07/13:762 about the production of endotoxin free ovalbumin by a German company now reveals that nearly all commercially available ovalbumin preparations are highly contaminated with endotoxin. Company A included 723, company B 1038, company C 257 and company D 342 EU/mg LPS. As all mice are usually also on a vitamin D supplement diet, recent mouse studies may have produced largely artifacts if both – agonist and antagonist – are included in an uncontrolled manner, yea, yea.
It is certainly hard to understand how early life events are leading to later disease. Here is an incredible nutrigenomics story done in agouti mice:
We find that the somatic epigenetic state of Avy is affected by in utero methyl donor supplementation only when the allele is paternally contributed. Exposure to methyl donor supplementation during midgestation shifts Avy phenotypes not only in the mice exposed as fetuses, but in their offspring. This finding indicates that methyl donors can change the epigenetic state of the Avy allele in the germ line, and that the altered state is retained through the epigenetic resetting that takes place in gametogenesis and embryogenesis. Thus a mother’s diet may have an enduring influence on succeeding generations.