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Background: Previously, D-Tryptophan has been identified as soluble bacterial molecule with Th2-lowering activity in vitro from prebiotic supernatants using bioassay-guided fractionation. However, the in vivo effects of D-Tryptophan on Th2-mediated disease are unknown. Here, we studied the effects of oral D-Tryptophan supplementation on allergic airway inflammation in mice. Methods: Six - eight weeks old female Balb/c mice received 50mM D-tryptophan (Sigma Aldrich, Germany) dissolved in the filtered drinking water or filtered drinking water as control (n=8 per group) starting at least 3 days before the first sensitization until sacrificing on day 25. An ovalbumin model with 3 intraperitoneal sensitizations (d0, d7, 14) and 3 intranasal challenges (d21, 22, 23) was applied to induce allergic airway inflammation. Results: Oral supplementation of mice with D-tryptophan significantly increased D-tryptophan serum levels indicating enteric uptake and systemic distribution. Pre-treatment of mice with D-tryptophan for 3 days and throughout experimental “asthma” induction lowered total BALF cells (from 9.1±1.9x10 5 to 4.4±0.5x10 5 cells), which was mainly caused by reduced eosinophils. Furthermore, D-Tryptophan treated mice exhibited less airway hyperreactivity than controls. Analysis of splenocytes revealed that D-tryptophan significantly reduced IL-13 and trendwise IL-4 (p=0.07) producing CD3 + CD4 + T cells, while IFNg + , Foxp3 + and IL-10 + T cells remained unchanged. In addition, the percentages of CD40 + and CD86 + DCs were reduced by half. Conclusion: Oral D-tryptophan supplementation reduces allergic airway inflammation in mice. Further studies are needed to provide insights into the mechanism of action.