Dermal injury drives a skin to gut axis that disrupts the intestinal microbiome and intestinal immune homeostasis in miceOriginal paper
What was studied?
Gallo and colleagues at UC San Diego asked whether injury to the skin, rather than the gut, could remotely alter intestinal microbes and immune function in mice. They used skin wounding and a transgenic model that digests dermal hyaluronan to isolate this direction of communication.
How was it studied?
Mice received full thickness skin wounds or expressed hyaluronidase in skin, then colon tissue was profiled by single cell and spatial RNA sequencing and fecal DNA by shotgun metagenomics. Causality was tested with oral vancomycin, germ free mice, and fecal microbiome transplantation into unwounded germ free mice before DSS colitis challenge.
What did they find?
Skin injury increased colon expression of host defense genes Reg3 and Muc2, changed gut bacterial composition and diversity, and let surviving bacteria penetrate the intestinal epithelium. Hyaluronan fragments released from injured skin directly induced Reg3 and Muc2 in cultured colon tissue and cells, and transplanting stool from wounded mice transferred the increased colitis susceptibility to unwounded germ free mice.
Why it matters
The findings reverse the usual assumption that gut microbes drive skin disease, showing skin damage can instead disrupt gut microbiome homeostasis and worsen intestinal inflammation. This supports a bidirectional skin-gut axis relevant to the clinical overlap between skin conditions like psoriasis and inflammatory bowel disease.