Atopic dermatitis (AD) is a chronic inflammatory dermatosis driven by skin barrier dysfunction, immune dysregulation, and gut–skin axis imbalance. While probiotics show promise, the therapeutic potential and mechanisms of topical postbiotics in modulating the gut–skin axis remain understudied. Here, we investigated the efficacy of Schleiferilactobacillus harbinensis JNDM-derived cell-free supernatant (CFS) and lysate (ShL) in a DNFB-induced AD mouse model. Topical application of both CFS and ShL significantly attenuated AD-like symptoms, reduced epidermal thickening, and restored the expression of the barrier protein filaggrin. Immunologically, treatment suppressed the Th2-dominant inflammatory cascade (IL-4, IL-5, IL-13, IL-33, TSLP) and reduced serum IgE and IFN-γ levels. Notably, ShL exhibited superior systemic efficacy, significantly inhibiting mast cell infiltration and reducing the spleen index. 16S rRNA sequencing revealed that topical intervention remotely remodeled the gut microbiota, specifically reversing the depletion of the beneficial genus Alistipes and suppressing the compensatory increase in Odoribacter. This microbial restructuring was accompanied by distinct metabolic changes: ShL treatment resulted in an approximately 4-fold elevation in fecal butyrate concentrations compared with the model group. Correlation analysis further validated a strong positive axis linking Alistipes abundance and butyrate levels to skin barrier integrity. Collectively, our findings demonstrate that S. harbinensis postbiotics—particularly the lysate—ameliorate AD through a dual mechanism of local barrier repair and systemic metabolic modulation via the gut–skin axis, presenting a promising non-steroidal therapeutic strategy.