Data from: Rapid environmental effects on gut nematode susceptibility in rewilded mice

Genetic and environmental factors shape host susceptibility to
infection, but how and how rapidly environmental variation might alter
the susceptibility of mammalian genotypes remains unknown. Here we
investigate the impacts of semi-natural environments upon the nematode
susceptibility profiles of inbred C57BL/6 mice. We hypothesized that
natural exposure to microbes might directly (e.g., via trophic
interactions) or indirectly (e.g., via microbe-induced immune
responses) alter the hatching, growth, and survival of nematodes in
mice housed outdoors. We found that while C57BL/6 mice are resistant
to high doses of nematode (Trichuris muris) eggs under clean
laboratory conditions, exposure to outdoor environments significantly
increased their susceptibility to infection, as evidenced by increased
worm burdens and worm biomass. Indeed, mice kept outdoors harbored as
many worms as STAT6 knockout mice, which are genetically deficient in
the type 2 immune response essential for clearing nematodes. Using 16S
ribosomal-RNA sequencing of fecal samples, we discovered enhanced
microbial diversity and specific bacterial taxa predictive of nematode
burden in outdoor mice. We also observed decreased type 2 and
increased type 1 immune responses in lamina propria and mesenteric
lymph node cells from infected mice residing outdoors. Importantly, in
our experimental design, different groups of mice received nematode
eggs either before or after moving outdoors. This contrasting timing
of rewilding revealed that enhanced hatching of worms was not
sufficient to explain the increased worm burdens; instead, microbial
enhancement and type 1 immune facilitation of worm growth and
survival, as hypothesized, were also necessary to explain our results.
These findings demonstrate that environment can rapidly and
significantly shape gut microbial communities and mucosal responses to
nematode infections, leading to variation in parasite expulsion rates
among genetically similar hosts.