Early-Life Intervention with Bifidobacterium longum subsp. infantis CCFM1269 Alleviates Atopic Dermatitis in Mice via the Indole-3-Lactic Acid-AHR Signaling Pathway.

Atopic dermatitis (AD) is a prevalent early childhood inflammatory skin disease frequently linked to gut dysbiosis. While Bifidobacterium longum subsp. infantis is a pioneer infant gut colonizer driving immune maturation, its role in AD prevention remains unclear. Here, we investigated early life intervention with B. longum subsp. infantis CCFM1269 using a 2,4-dinitrofluorobenzene (DNFB)-induced murine AD model. Oral administration of CCFM1269 significantly ameliorated AD symptoms, reducing skin/ear thickness, dermatitis scores, and serum IgE. Mechanistically, CCFM1269 modulated the systemic Th1/Th2 balance by downregulating TSLP, IL-4, and IL-13, while upregulating IFN-γ. Notably, CCFM1269 produced indole-3-lactic acid (ILA). Via the gut-skin axis, ILA activated the aryl hydrocarbon receptor (AHR) and its target CYP1A1 in skin tissues, strengthening the epidermal barrier. Additionally, AD mitigation was associated with gut microbiota reshaping. Ultimately, CCFM1269 alleviates AD primarily through the ILA- AHR signaling pathway, highlighting its potential as a functional food ingredient for early life AD prevention.