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In this study, we investigated the signalling pathways mediating tryptophan (Trp)-promoted β-defensin-2 (BD-2) expression in rat intestinal mucosa. Sprague Dawley rats were administered with l-Trp and treated with rapamycin (RAPA), 1-methyltryptophan (1-MT), or para -chlorophenyl-amine (PCPA) to inhibit mammalian target of rapamycin (mTOR), indoleamine-2,3-dioxygenase (IDO), or tryptophan hydroxylase (TPH), respectively. The mRNA and protein levels of BD-2 in the jejunal and ileal mucosa of rats increased with administration of l-Trp. Intraperitoneal injection of RAPA significantly decreased the mRNA level of BD-2 and the concentrations of p -mTORC1 and BD-2 in the jejunal and ileal mucosa of rats with administration of l-Trp ( P &lt; 0.05). Oral administration of 1-MT decreased the IDO activity and the mRNA and protein levels of BD-2, and increased the concentrations of tumour necrosis factor (TNF-α), interleukin (IL)-17, and IL-22 in the jejunal and ileal mucosa of rats with administration of l-Trp ( P &lt; 0.05). Intraperitoneal injection of PCPA decreased the TPH activity and increased the mRNA and protein levels of BD-2, but did not change the concentrations of TNF-α, IL-17, or IL-22 in the jejunal and ileal mucosa of rats with administration of l-Trp. The results indicate the Trp-promoted BD-2 expression in the jejunum and ileum via the mTOR pathway and its metabolites: kynurenine banding to aryl hydrocarbon receptor in rat intestine.

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Tryptophan promoted β-defensin-2 expression<i>via</i>the mTOR pathway and its metabolites: kynurenine banding to aryl hydrocarbon receptor in rat intestine

Tryptophan promoted β-defensin-2 expressionviathe mTOR pathway and its metabolites: kynurenine banding to aryl hydrocarbon receptor in rat intestine