D-tryptophan from probiotic bacteria influences allergic airway disease
The prevalence of chronic immune diseases such as asthma is on the increase. Current available pharmaceuticals show improvement of symptoms, however the underlying pathologies remain unaddressed. Alternatives to pharmaceutical products are of increasing demand and probiotics have been suggested for the primary prevention and/or treatment of immune diseases including allergic diseases. Nevertheless, clinical trials yielded inconsistent results possibly due to the complex interaction among probiotic bacteria, the human microbiome and the host.
This study aimed to identify and characterize a bioactive, probiotic metabolite with immune modulatory activity for potential prevention of allergic airway disease.
A wide range of different probiotic bacteria (37 in total) was selected for use in this study of which 11 were Winclove strains. Probiotic supernatants were screened for their ability to lower the secretion of CCL17 in human Tcells, a Th2-induced chemokine, and to prevent the expression of co-stimulatory molecules on human dendritic cells. Immunoactivity was expressed by 13 probiotic supernatants and two of these were selected for further fractionation yielding to a putative bioactive substance. ProtonNMR techniques identified the bioactive substance as D-tryptophan.
To study the ability of D-tryptophan to ameliorate asthma, a mouse model of induced asthma was used. When feeding mice with D-tryptophan prior to experimental asthma induction, airway resistance was reduced, increased numbers of gut foxp3+ T cells, lowered systemic Th2 responses and ameliorated allergic airway inflammation and hyperresponsiveness. Moreover, D-tryptophan restored the gut microbal diversity, which was distorted during allergic airway inflammation.
All in all, bacterial D-tryptophan is able to shape mammalian immune responses and the intestinal microbiota, which could contribute to the improvement of experimental asthma symptoms.
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