Our Projects

Across 1,068 participants in a 3-year, four-country study, scalp microbiome patterns track alopecia severity, progression, and treatment response. We built the Hair Microbiome Health Index (HMHI) to flag and predict disease course. A multi-omics Microbe–Metabolites–Host Crosstalk model shows Cutibacterium acnes converts tryptophan to indole, overactivating AHR in sebocytes, triggering CXCL12 release, recruiting CXCR4+ NKT cells, and stalling follicle growth. Targeting microbe–host signaling offers a therapeutic path for hair loss.

Exercise offers nearly universal benefits to organs throughout the body, yet its effects on the skin remain largely unexplored. By collecting skin samples from an exercise cohort and establishing a voluntary exercise mouse model, we demonstrated that exercise possesses both preventive and therapeutic effects against chronic inflammatory skin diseases. Exercise shapes a unique skin microbiome by regulating glandular secretion, significantly increasing colonization by Staphylococcus epidermidis (S. epidermidis) in physically active individuals. Concurrently, we discovered that exercise upregulates systemic lipid metabolism and substantially increases the secretion of tripalmitoleoylglycerol (TPG) into the epidermal lipid barrier. S. epidermidis hydrolyzes this glyceride via lipase to produce palmitoleic acid (POA), and this small molecule metabolite activates the PPARγ-DGAT2 signaling pathway in keratinocytes to protect the skin barrier. This reveals that exercise modulates lipid metabolism in the host and the skin microenvironment, offering novel insights into exercise interventions for chronic inflammatory skin diseases.

When the ancestors of humans ventured onto land hundreds of millions of years ago, exposure to air simultaneously altered the host's lung and skin microbiota. Evolution shaped the cross-organ tolerance of host immune system to commensals, which in turn regulate excessive immune responses in the host. Through multi-center cohort studies and mouse models, we demonstrated that in atopic dermatitis, skin commensal Staphylococcus epidermidis (S. epidermidis) produces indole-3-lactic acid (ILA) to activate aryl hydrocarbon receptor (AhR) in the lung via systemic circulation. This activation dependently increases lung commensal Rothia mucilaginosa (R. mucilaginosa) abundance, elevating short-chain fatty acids (SCFAs) concentration in the lung environment to alleviate atopic march (the progression from atopic dermatitis to allergic asthma). These findings identify a conserved cross-organ microbial adaptive evolution strategy against excessive host immunity, offering clues for therapies targeting inter-organ bacterial crosstalk in immune regulation.