Back

A lipid-driven, microbe-independent mechanism of acne via Lrig1+ follicular progenitor cells

Sugihira, T.; Tamai, M.; Takagi, K.; Salcman, B.; Kobayashi, T.; Hobro, A. J.; Nakagawa, S.; Takeuchi, Y.; Ishikawa, E.; Maekawa, M.; Owada, Y.; Inohara, N.; Takahashi, H.; Smith, N. I.; Yamasaki, S.; Fujimoto, M.; Nakamura, Y.

2025-08-31 cell biology
10.1101/2025.08.30.673221 bioRxiv
Show abstract

Long-chain saturated fatty acids (lcSFAs) are abundant in the skin, but their pathogenic roles in acne remain unclear. In human sebum profiling, C16:0, the most abundant lcSFA, was the only fatty acid significantly elevated in acne and correlated with inflammatory comedone counts. We then established a mouse model that faithfully recapitulates human acne phenotypes, in which topical C16:0 penetrated the epidermis and induced sebocyte hyperplasia, comedogenesis, and follicular inflammation. Mechanistically, C16:0 activated keratinization and inflammatory pathways and drove sebocyte-lineage differentiation from Lrig1+progenitor cells, which function as cutaneous lipid sensors. These effects persisted in germ-free mice and were unaffected by fatty acid transporter modulation, while MyD88 signaling was partially required for inflammatory cell recruitment. Together, our findings identified C16:0 as a human acne-associated lipid that recapitulates disease hallmarks through a microbe-independent, lipid-driven pathway, highlighting Lrig1+cells as central hubs in remodeling of the pilosebaceous unit.

Matching journals

The top 5 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.