Skip to main content
ARS Home » Midwest Area » West Lafayette, Indiana » Livestock Behavior Research » Research » Publications at this Location » Publication #323505

Title: Effect of threonine deficiency on intestinal integrity and immune response to coccidiosis in broiler chicks

item ZHANG, QIAN - Purdue University
item CHEN, XI - Purdue University
item Eicher, Susan
item AJUWON, KOLAPO - Purdue University
item APPLEGATE, JOHN - Purdue University

Submitted to: International Poultry Scientific Forum
Publication Type: Abstract Only
Publication Acceptance Date: 12/12/2015
Publication Date: 1/26/2016
Citation: Zhang, Q., Chen, X., Eicher, S.D., Ajuwon, K., Applegate, J. 2016. Effect of threonine deficiency on intestinal integrity and immune response to coccidiosis in broiler chicks. International Poultry Scientific Forum. p.33.

Interpretive Summary:

Technical Abstract: We hypothesized that threonine (Thr) deficiency would exacerbate the intestinal damage induced by feed withdraw combined with coccidiosis, because of its high obligatory requirement by the gut. In this study, two dietary Thr treatments (0.49 and 0.90%) were fed to chicks from 1-21 d of age. At 13 d of age, feed was withdrawn for 24 h from half of the birds for each treatment with subsequent gavage of a 25×-recommended dose of Coccivac®-B. Samples were collected at 21 d of age. Thr deficiency or combined challenge decreased BW gain and feed intake as well as increased feed to gain from 13 to 21 d of age (P = 0.03). BW gain was lowest in challenged birds receiving the low Thr diet (Thr × challenge, P = 0.03). Also, the lowest villus height (VH) and VH:crypt depth (CD) in the challenged birds with 0.49% Thr was observed in jejunum (Thr × challenge, P = 0.07), which may partially account for their lowest BW gain. The dramatically increased CD in the challenged birds (P < 0.01) indicated intestinal epithelial proliferation, and thus a plausible mechanism for intestinal oocyst expulsion and intestinal repair, as the challenged group fed 0.49% Thr had higher numbers of oocysts (+40%, P = 0.03) but lower CD (-31%, P < 0.01). Additionally, birds with 0.49% Thr diet had higher gut permeability as measured after 2 h administration of FITC-dextran (3-5 kDa, P < 0.01), which may be attributed to decreased IgA production (P = 0.10) in ileum. In the cecal tonsils, Thr deficienct birds had a lower percentage of lymphocytes expressing CD4, CD8, CD3 and Bu-1 regardless of challenge (P = 0.01), along with the lower mRNA expression of the chemokine receptor CCR9 for gut homing T cells and B cells (P < 0.01). Although the challenge increased all the above lymphocyte proportions (P = 0.05), the limited increase of CD3 lymphocyte (49% of Bu-1 lymphocytes) for the 0.49% Thr group induced the lowest CD3 to Bu-1 ratio (Thr × challenge, P = 0.09). Consistently, the gene expression of IFN-' was lower in the 0.49% Thr group compared to the 0.90% Thr group under challenge (Thr × challenge, P = 0.06). Overall, Thr deficiency worsened the detrimental effects on growth performance of coccidiosis by compromising oocyst shedding, intestinal morphology, barrier function, lymphocyte profiles and IFN-' expression. These results show the benefit of maintaining Thr concentrations for protecting poultry from coccidian.