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. 2019 May 22;9(1):7689.
doi: 10.1038/s41598-019-44205-3.

Dietary tryptophan deficiency and its supplementation compromises inflammatory mechanisms and disease resistance in a teleost fish

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Dietary tryptophan deficiency and its supplementation compromises inflammatory mechanisms and disease resistance in a teleost fish

M Machado et al. Sci Rep. .

Abstract

Tryptophan participates on several physiological mechanisms of the neuroendocrine-immune network and plays a critical role in macrophages and lymphocytes function. This study intended to evaluate the modulatory effects of dietary tryptophan on the European seabass (Dicentrarchus labrax) immune status, inflammatory response and disease resistance to Photobacterium damselae piscicida. A tryptophan deficient diet (NTRP); a control diet (CTRL); and two other diets supplemented with tryptophan at 0.13% (TRP13) and 0.17% (TRP17) of feed weight were formulated. Fish were sampled at 2 and 4 weeks of feeding and the remaining were i.p. injected with Phdp (3 × 106 cfu/fish) at 4 weeks and the inflammatory response (at 4, 24, 48 and 72 hours post-infection) as well as survival were evaluated. Results suggest that fish immune status was not altered in a tryptophan deficient scenario whereas in response to an inflammatory insult, plasma cortisol levels increased and the immune cell response was compromised, which translated in a lower disease resistance. When dietary tryptophan was offered 30% above its requirement level, plasma cortisol increased and, in response to bacterial infection, a decrease in lymphocytes, monocytes/macrophages and several immune-related genes was observed, also compromising at some degree fish disease resistance.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
Cumulative mortality (%) of European seabass fed NTRP (formula image), CTRL (formula image), TRP 13 (formula image) and TRP 17 (formula image) for 4 weeks and subsequently infected with Phdp (n = 60).
Figure 2
Figure 2
Quantitative expression of (A) interlukin-10, (B) interleukin-8; (C) transforming growth factor β, (D) superoxide dismutase, (E) interferon-γ, (F) heat shock protein 90, (G) metalloproteinase 9, (H) glucocorticoid receptor 1 and (I) indoleamine 2,3- dioxygenase genes in the head-kidney of European seabass fed dietary treatments prior infection, and at 4, 24, 48 and 72 h after peritoneal infection with Phdp. Values are presented as means ± SD (n = 6). P-values from two-way ANOVA (p ≤ 0.05). If interaction was significant, Tukey post hoc test was used to identify differences in the experimental treatments. Different lowercase letters stand for significant differences among dietary treatments for the same time while different symbols stand for significant differences between times for the same diet.
Figure 3
Figure 3
Experimental design.

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